Reviewer #1 (Public Review):

Summary:

Li et al investigated how adjuvants such as MPLA and CpG influence antigen presentation at the level of the Antigen-presenting cell and MHCII : peptide interaction. They found that the use of MPLA or CpG influences the exogenous peptide repertoire presented by MHC II molecules. Additionally, their observations included the finding that peptides with low-stability peptide:MHC interactions yielded more robust CD4+ T cell responses in mice. These phenomena were illustrated specifically for 2 pattern recognition receptor activating adjuvants. This work represents a step forward for how adjuvants program CD4+ Th responses and provides further evidence regarding the expected mechanisms of PRR adjuvants in enhancing CD4+ T cell responses in the setting of vaccination.

Strengths:

The authors use a variety of systems to analyze this question. Initial observations were collected in an H pylori model of vaccination with a demonstration of immunodominance differences simply by adjuvant type, followed by analysis of MHC:peptide as well as proteomic analysis with comparison by adjuvant group. Their analysis returns to peptide immunization and analysis of strength of relative CD4+ T cell responses, through calculation of IC:50 values and strength of binding. This is a comprehensive work. The logical sequence of experiments makes sense and follows an unexpected observation through to trying to understand that process further with peptide immunization and its impact on Th responses. This work will premise further studies into the mechanisms of adjuvants on T cells

Weaknesses:

While MDP has a different manner of interaction as an adjuvant compared to CpG and MPLA, it is unclear why MDP has a different impact on peptide presentation and it should be further investigated, or at minimum highlighted in the discussion as an area that requires further investigation.

It is alluded by the authors that TLR activating adjuvants mediate selective, low affinity, exogenous peptide binding onto MHC class II molecules. However, this was not demonstrated to be related specifically to TLR binding. I wonder if some work with TLR deficient mice (TLR 4KO for example) could evaluate this phenomenon more specifically.

It is unclear to me if this observation is H pylori model/antigen-specific. It may have been nice to characterize the phenomenon with a different set of antigens as supplemental. Lastly, it is unclear if the peptide immunization experiment reveals a clear pattern related to high and low-stability peptides among the peptides analyzed.

Reviewer #2 (Public Review):

Adjuvants boost antigen-specific immune responses to vaccines. However, whether adjuvants modulate the epitope immunodominance and the mechanisms involved in adjuvant's effect on antigen processing and presentation are not fully characterized. In this manuscript, Li et al report that immunodominant epitopes recognized by antigen-specific T cells are altered by adjuvants.

Using MPLA, CpG, and MDP adjuvants and H. pylori antigens, the authors screened the dominant epitopes of Th1 responses in mice post-vaccination with different adjuvants and found that adjuvants altered antigen-specific CD4+ T cell immunodominant epitope hierarchy. They show that adjuvants, MPLA and CpG especially, modulate the peptide repertoires presented on the surface of APCs. Surprisingly, adjuvant favored the presentation of low-stability peptides rather than high-stability peptides by APCs. As a result, the low stability peptide presented in adjuvant groups elicits T cell response effectively.

eLife assessment

This study provides valuable insights into how IL-1 cytokines may protect cells against SARS-COV-2 infection. By inducing a non-canonical RhoA/ROCK signaling pathway, IL-1beta appears to inhibit the ability of SARS-COV-2 infected cells to fuse with uninfected cells and produce syncytia. The evidence underlying the identification of the key signaling components required for this inhibitory phenotype in vitro is solid and could be further improved by addressing key weaknesses. However, data supporting this specific mechanism of inhibition in IL-1-mediated control of SARS-COV-2 infection in vivo remains incomplete.

Reviewer #1 (Public Review):

Summary:

SARS-CoV-2 infection induces syncytia formation, which promotes viral transmission. In this paper, the authors aimed to understand how host-derived inflammatory cytokines IL-1α/β combat SARS-CoV-2 infection.

Strengths:

First, they used a cell-cell fusion assay developed previously to identify IL-1α/β as the cytokines that inhibit syncytia formation. They co-cultured cells expressing the spike protein and cells expressing ACE2 and found that IL-1β treatment decreased syncytia formation and S2' cleavage.

Second, they investigated the IL-1 signaling pathway in detail, using knockouts or pharmacological perturbation to understand the signaling proteins responsible for blocking cell fusion. They found that IL-1 prevents cell-cell fusion through MyD88/IRAK/TRAF6 but not TAK1/IKK/NF-κB, as only knocking out MyD88/IRAK/TRAF6 eliminates the inhibitory effect on cell-cell fusion in response to IL-1β. This revealed that the inhibition of cell fusion did not require a transcriptional response and was mediated by IL-1R proximal signaling effectors.

Third, the authors identified RhoA/ROCK activation by IL-1 as the basis for this inhibition of cell fusion. By visualizing a RhoA biosensor and actin, they found a redistribution of RhoA to the cell periphery and cell-cell junctions after IL-1 stimulation. This triggered the formation of actin bundles at cell-cell junctions, preventing fusion and syncytia formation. The authors confirmed this molecular mechanism by using constitutively active RhoA and an inhibitor of ROCK.

Diverse Cell types and in vivo models were used, and consistent results were shown across diverse models. These results were convincing and well-presented.

Weaknesses:

As the authors point out in the discussion, whether IL-1-mediated RhoA activation is specific to viral infection or regulates other RhoA-regulated processes is unclear. We would also require high-magnification images of the subcellular organization of the cytoskeleton to appreciate the effect of IL-1 stimulation.

Reviewer #2 (Public Review):

Summary:

In this study, Zheng et al investigated the role of inflammatory cytokines in protecting cells against SARS-CoV-2 infection. They demonstrate that soluble factors in the supernatants of TLR-stimulated THP1 cells reduce fusion events between HEK293 cells expressing SARS-CoV-2 S protein and the ACE2 receptor. Using qRT-PCR and ELISA, they demonstrate that IL-1 cytokines are (not surprisingly) upregulated by TLR treatment in THP1 cells. Further, they convincingly demonstrate that recombinant IL-1 cytokines are sufficient to reduce cell-to-cell fusion mediated by the S protein. Using chemical inhibitors and CRISPR knock-out of key IL-1 receptor signaling components in HEK293 cells, they demonstrate that components of the myddosome (MYD88, IRAK1/4, and TRAF6) are required for fusion inhibition, but that downstream canonical signaling (i.e., TAK1 and NFKB activation) is not required. Instead, they provide evidence that IL-1-dependent non-canonical activation of RhoA/Rock is important for this phenotype. Importantly, the authors demonstrate that expression of a constitutively active RhoA alone is sufficient to inhibit fusion and that chemical inhibition of Rock could reverse this inhibition. The authors followed up these in vitro experiments by examining the effects of IL-1 on SARS-COV-2 infection in vivo and they demonstrate that recombinant IL-1 can reduce viral burden and lung pathogenesis in a mouse model of infection. However, the contribution of the RhoA/Rock pathway and inhibition of fusion to IL-1-mediated control of SARS-CoV-2 infection in vivo remains unclear.

Strengths:

(1) The bioluminescence cell-cell fusion assay provides a robust quantitative method to examine cytokine effects on viral glycoprotein-mediated fusion.

(2) The study identifies a new mechanism by which IL-1 cytokines can limit virus infection.

(3) The authors tested IL-1 mediated inhibition of fusion induced by many different coronavirus S proteins and several SARS-CoV-2 strains.

Weaknesses:

(1) The qualitative assay demonstrating S2 cleavage and IL-1 mediated inhibition of this phenotype is extremely variable across the data figures. Sometimes it appears like S2 cleavage (S2') is reduced, while in other figures immunoblots show that total S2 protein is decreased. Based on the proposed model the expectation would be that S2 abundance would be rescued when cleavage is inhibited.

(2) The text referencing Figure 1H suggests that TLR-stimulated THP-1 cell supernatants "significantly" reduce syncytia, but image quantification and statistics are not provided to support this statement.

(3) The authors conclude that because IL-1 accumulates in TLR2-stimulated THP1 monocyte supernatants, this cytokine accounts for the ability of these supernatants to inhibit cell-cell fusion. However, they do not directly test whether IL-1 is required for the phenotype. Inhibition of the IL-1 receptor in supernatant-treated cells would help support their conclusion.

(4) Immunoblot analysis of IL-1 treated HEK293 cells suggests that this cytokine does not reduce the abundance of ACE2 or total S protein in cells. However, it is possible that IL-1 signaling reduces the abundance of these proteins on the cell surface, which would result in a similar inhibition of cell-cell fusion. The authors should confirm that IL-1 treatment of their cells does not change Ace2 or S protein on the cell surface.

(5) In Figure 5A, expression of constitutively active RhoA appears to have profound effects on how ACE2 runs by SDS-PAGE, suggesting that RhoA may have additional effects on ACE2 biology that might account for the decreased cell-cell fusion. This phenotype should be addressed in the text and explored in more detail.

(6) The experiments linking IL-1 mediated restriction of SARS-COV-2 fusion to the control of virus infection in vivo are incomplete. The reported data demonstrate that recombinant IL-1 can restrict virus replication in vivo, but they fall short of confirming that the in vitro mechanism described (reduced fusion) contributes to the control of SARS-CoV2 replication in vivo. A critical piece of data that is missing is the demonstration that the ROCK inhibitor phenocopies IL-1RA treatment of SARS-COV-2 infected mice (viral infection and pathology).

eLife assessment

In this valuable study, the authors propose a model wherein the bacterial redox state plays a crucial role in the differentiation of Chlamydia trachomatis into elementary and reticulate bodies. They provide evidence to argue that a highly oxidising environment favours the formation of elementary bodies while a reducing condition slows down development. Whilst aspects related to the role of AhpC in regulating redox, and implications on differentiation, are solid, more precise measurements of the redox potential are required to convincingly demonstrate the role of redox in developmental progression.

Reviewer #1 (Public Review):

Summary:

Chlamydia spp. has a biphasic developmental cycle consisting of an extracellular, infectious form called an elementary body (EB) and an intracellular, replicative form known as a reticular body (RB). The structural stability of EBs is maintained by extensive cross-linking of outer membrane proteins while the outer membrane proteins of RBs are in a reduced state. The overall redox state of EBs is more oxidized than RBs. The authors propose that the redox state may be a controlling factor in the developmental cycle. To test this, alkyl hydroperoxide reductase subunit C (ahpC) was overexpressed or knocked down to examine effects on developmental gene expression. KD of ahpC induced increased expression of EB-specific genes and accelerated EB production. Conversely, overexpression of phpC delayed differentiation to EBs. The results suggest that chlamydial redox state may play a role in differentiation.

Strengths:

Uses modern genetic tools to explore the difficult area of temporal gene expression throughout the chlamydial developmental cycle.

Weaknesses:

The environmental signals triggering ahpC expression/activity are not determined.

Reviewer #2 (Public Review):

The factors that influence the differentiation of EBs and RBs during Chlamydial development are not clearly understood. A previous study had shown a redox oscillation during the Chlamydial developmental cycle. Based on this observation, the authors hypothesize that the bacterial redox state may play a role in regulating the differentiation in Chlamydia. To test their hypothesis, they make knock-down and overexpression strains of the major ROS regulator, ahpC. They show that the knock-down of ahpC leads to a significant increase in ROS levels leading to an increase in the production of elementary bodies and overexpression leads to a decrease in EB production likely caused by a decrease in oxidation. From their observations, they present an interesting model wherein an increase in oxidation favors the production of EBs.

Major concern:

In the absence of proper redox potential measurements, it is not clear if what they observe is a general oxidative stress response, especially when the knock-down of ahpC leads to a significant increase in ROS levels. Direct redox potential measurement in the ahpC overexpression and knock-down cells is required to support the model. This can be done using the roGFP-based measurements mentioned in the Wang et al. 2014 study cited by the authors.

Reviewer #3 (Public Review):

Summary:

The study reports clearly on the role of the AhpC protein as an antioxidant factor in Chlamydia trachomatis and speculates on the role of AhpC as an indirect regulator of developmental transcription induced by redox stress in this differentiating obligate intracellular bacterium.

Strengths:

The question posed and the concluding model about redox-dependent differentiation in chlamydia is interesting and highly relevant. This work fits with other propositions in which redox changes have been reported during bacterial developmental cycles, potentially as triggers, but have not been cited (examples PMID: 2865432, PMID: 32090198, PMID: 26063575). Here, AhpC over-expression is shown to protect Chlamydia towards redox stress imposed by H2O2, CHP, TBHP, and PN, while CRISPRi-mediated depletion of AhpC curbed intracellular replication and resulted in increased ROS levels and sensitivity to oxidizing agents. Importantly, the addition of ROS scavengers mitigated the growth defect caused by AhpC depletion. These results clearly establish the role of AhpC affects the redox state and growth in Ct (with the complicated KO genetics and complementation that are very nicely done).

Weaknesses:

However, with respect to the most important implication and claims of this work, the role of redox in controlling the chlamydial developmental cycle rather than simply being a correlation/passenger effect, I am less convinced about the impact of this work. First, the study is largely observational and does not resolve how this redox control of the cell cycle could be achieved, whereas in the case of Caulobacter, a clear molecular link between DNA replication and redox has been proposed. How would progressive oxidation in RBs eventually trigger the secondary developmental genes to induce EB differentiation? Is there an OxyR homolog that could elicit this change and why would the oxidation stress in RBs gradually accumulate during growth despite the presence of AhpC? In other words, the role of AhpC is simply to delay or dampen the redox stress response until the trigger kicks in, again, what is the trigger? Is this caused by increasing oxidative respiration of RBs in the inclusion? But what determines the redox threshold?

I also find the experiment with Pen treatment to have little predictive power. The fact that transcription just proceeds when division is blocked is not unprecedented. This also happens during the Caulobacter cell cycle when FtsZ is depleted for most developmental genes, except for those that are activated upon completion of the asymmetric cell division and that is dependent on the completion of compartmentalization. This is a smaller subset of developmental genes in caulobacter, but if there is a similar subset that depends on division on chlamydia and if these are affected by redox as well, then the argument about the interplay between developmental transcription and redox becomes much stronger and the link more intriguing. Another possibility to strengthen the study is to show that redox-regulated genes are under the direct control of chlamydial developmental regulators such as Euo, HctA, or others and at least show dual regulation by these inputs -perhaps the feed occurs through the same path.

This redox-transcription shortcoming is also reflected in the discussion where most are about the effects and molecular mitigation of redox stress in various systems, but there is little discussion on its link with developmental transcription in bacteria in general and chlamydia.

eLife assessment

This important study examines the role of TNF in modulating energy metabolism during parasite infection. The authors perform an elegant set of studies, however the evidence supporting the major claims of the manuscript is incomplete. This work integrates an interesting set of observations that will be of interest to the Plasmodium and pathogenesis communities with an expanded set of experiments.

Reviewer #1 (Public Review):

Summary:

The manuscript by Kely C. Matteucc et al. titled "Reprogramming of host energy metabolism mediated by the TNF-iNOS-HIF-1α axis plays a key role in host resistance to Plasmodium infection" describes that TNF induces HIF-1α stabilization that increases GLUT1 expression as well as glycolytic metabolism in monocytic and splenic CD11b+ cells in P. chabaudi infected mice. Also, TNF signaling plays a crucial role in host energy metabolism, controlling parasitemia, and regulating the clinical symptoms in experimental malaria.

Weaknesses:

Even though iNOS deficiency reduced the expression of the glycolytic enzymes as well as reduced GLUT1 expression and lower ECAR in splenic monocytes, there is no data to support that RNI induces the expression and stabilization of HIF-1α.

This paper involves an incredible amount of work, and the authors have done an exciting study addressing the TNF-iNOS-HIF-1α axis as a critical role in host immune defense during Plasmodium infection.

Reviewer #2 (Public Review):

Summary:

The premise of the manuscript by Matteucci et al. is interesting and elaborates on a mechanism via which TNFa regulates monocyte activation and metabolism to promote murine survival during Plasmodium infection. The authors show that TNF signaling (via an unknown mechanism) induces nitrite synthesis, which (via yet an unknown mechanism), and stabilizes the transcription factor HIF1a. Furthermore, HIF1a (via an unknown mechanism) increases GLUT1 expression and increases glycolysis in monocytes. The authors demonstrate that this metabolic rewiring towards increased glycolysis in a subset of monocytes is necessary for monocyte activation including cytokine secretion, and parasite control.

Strengths:

The authors provide elegant in vivo experiments to characterize metabolic consequences of Plasmodium infection, and isolate cell populations whose metabolic state is regulated downstream of TNFa. Furthermore, the authors tie together several interesting observations to propose an interesting model.

Weaknesses:

The main conclusion of this work - that "Reprogramming of host energy metabolism mediated by the TNF-iNOS-HIF1a axis plays a key role in host resistance to Plasmodium infection" is unsubstantiated. The authors show that TNFa induces GLUT1 in monocytes, but never show a direct role for GLUT1 or glucose uptake in monocytes in host resistance to infection (nor the hypoglycemia phenotype they describe).

eLife assessment

The work provides a valuable assessment of how antibiotics impact the human gut microbiota in diverse observational cohorts. Although the data presented are solid, some of the assumptions underlying their models may have affected the interpretation of their findings. The study is relevant for researchers and clinicians interested in antimicrobial resistance.

Reviewer #1 (Public Review):

Summary:

In this manuscript, the authors provide a study among healthy individuals, general medical patients and patients receiving haematopoietic cell transplants (HCT) to study the gut microbiome through shotgun metagenomic sequencing of stool samples. The first two groups were sampled once, while the patients receiving HCT were sampled longitudinally. A range of metadata (including current and previous (up to 1 year before sampling) antibiotic use) was recorded for all sampled individuals. The authors then performed shotgun metagenomic sequencing (using the Illumina platform) and performed bioinformatic analyses on these data to determine the composition and diversity of the gut microbiota and the antibiotic resistance genes therein. The authors conclude, on the basis of these analyses, that some antibiotics had a large impact on gut microbiota diversity, and could select opportunistic pathogens and/or antibiotic resistance genes in the gut microbiota.

Strengths:

The major strength of this study is the considerable achievement of performing this observational study in a large cohort of individuals. Studies into the impact of antibiotic therapy on the gut microbiota are difficult to organise, perform and interpret, and this work follows state-of-the-art methodologies to achieve its goals. The authors have achieved their objectives and the conclusion they draw on the impact of different antibiotics and their impact on the gut microbiota and its antibiotic resistance genes (the 'resistome', in short), are supported by the data presented in this work.

Weaknesses:

The weaknesses are the lack of information on the different resistance genes that have been identified and which could have been supplied as Supplementary Data. In addition, no attempt is made to assess whether the identified resistance genes are associated with mobile genetic elements and/or (opportunistic) pathogens in the gut. While this is challenging with short-read data, alternative approaches like long-read metagenomics, Hi-C and/or culture-based profiling of bacterial communities could have been employed to further strengthen this work. Unfortunately, the authors have not attempted to perform corrections for multiple testing because many antibiotic exposures were correlated.

Impact:

The work may impact policies on the use of antibiotics, as those drugs that have major impacts on the diversity of the gut microbiota and select for antibiotic resistance genes in the gut are better avoided. However, the primary rationale for antibiotic therapy will remain the clinical effectiveness of antimicrobial drugs, and the impact on the gut microbiota and resistome will be secondary to these considerations.

Reviewer #2 (Public Review):

Summary:

In this manuscript by Peto et al., the authors describe the impact of different antimicrobials on gut microbiota in a prospective observational study of 225 participants (healthy volunteers, inpatients and outpatients). Both cross-sectional data (all participants) and longitudinal data (a subset of 79 haematopoietic cell transplant patients) were used. Using metagenomic sequencing, they estimated the impact of antibiotic exposure on gut microbiota composition and resistance genes. In their models, the authors aim to correct for potential confounders (e.g. demographics, non-antimicrobial exposures and physiological abnormalities), and for differences in the recency and total duration of antibiotic exposure. I consider these comprehensive models an important strength of this observational study. Yet, the underlying assumptions of such models may have impacted the study findings (detailed below). Other strengths include the presence of both cross-sectional and longitudinal exposure data and the presence of both healthy volunteers and patients. Together, these observational findings expand on previous studies (both observational and RCTs) describing the impact of antimicrobials on gut microbiota.

Weaknesses:

(1) The main weaknesses result from the observational design. This hampers causal interpretation and corrects for potential confounding necessary. The authors have used comprehensive models to correct for potential confounders and for differences between participants in duration of antibiotic exposure and time between exposure and sample collection. I wonder if some of the choices made by the authors did affect these findings. For example, the authors did not include travel in the final model, but travel (most importantly, south Asia) may result in the acquisition of AMR genes [Worby et al., Lancet Microbe 2023; PMID 37716364). Moreover, non-antimicrobial drugs (such as proton pump inhibitors) were not included but these have a well-known impact on gut microbiota and might be linked with exposure to antimicrobial drugs. Residual confounding may underlie some of the unexplained discrepancies between the cross-sectional and longitudinal data (e.g. for vancomycin).

In addition, the authors found a disruption half-life of 6 days to be the best fit based on Shannon diversity. If I'm understanding correctly, this results in a near-zero modelled exposure of a 14-day-course after 70 days (purple line; Supplementary Figure 2). However, it has been described that microbiota composition and resistome (not Shannon diversity!) remain altered for longer periods of time after (certain) antibiotic exposures (e.g. Anthony et al., Cell Reports 2022; PMID 35417701). The authors did not assess whether extending the disruption half-life would alter their conclusions.

(2) Another consequence of the observational design of this study is the relatively small number of participants available for some comparisons (e.g. oral clindamycin was only used by 6 participants). Care should be taken when drawing any conclusions from such small numbers.

(3) The authors assessed log-transformed relative abundances of specific bacteria after subsampling to 3.5 million reads. While I agree that some kind of data transformation is probably preferable, these methods do not address the compositional data of microbiome data and using a pseudocount (10-6) is necessary for absent (i.e. undetected) taxa [Gloor et al., Front Microbiol 2017; PMID 29187837]. Given the centrality of these relative abundances to their conclusions, a sensitivity analysis using compositionally-aware methods (such as a centred log-ratio (clr) transformation) would have added robustness to their findings.

(4) An overall description of gut microbiota composition and resistome of the included participants is missing. This makes it difficult to compare the current study population to other studies. In addition, for correct interpretation of the findings, it would have been helpful if the reasons for hospital visits of the general medical patients were provided.

eLife assessment

This valuable study reports data showing the link between a disruption in testicular mineral (phosphate) homeostasis, FGF23 expression, and Sertoli cell dysfunction. The data supporting the conclusion remains incomplete. This work will be of interest to biomedical researchers working on testis biology and male infertility.

Reviewer #1 (Public Review):

Summary:

Despite the study being a collation of important results likely to have an overall positive effect on the field, methodological weaknesses and suboptimal use of statistics make it difficult to give confidence to the study's message.

Strengths:

Relevant human and mouse models approached with in vivo and in vitro techniques.

Weaknesses:

The methodology, statistics, reagents, analyses, and manuscripts' language all lack rigour.

(1) The authors used statistics to generate P-values and Rsquare values to evaluate the strength of their findings.

However, it is unclear how stats were used and/or whether stats were used correctly. For instance, the authors write: "Gaussian distribution of all numerical variables was evaluated by QQ plots". But why? For statistical tests that fall under the umbrella of General Linear Models (line ANOVA, t-tests, and correlations (Pearson's)), there are several assumptions that ought to be checked, including typically:

(a) Gaussian distribution of residuals.

(b) Homoskedasticity of the residuals.

(c) Independence of Y, but that's assumed to be valid due to experimental design.

So what is the point of evaluating the Gaussian distribution of the data themselves? It is not necessary. In this reviewer's opinion, it is irrelevant, not a good use of statistics, and we ought to be leading by example here.

Additionally, it is not clear whether the homoscedasticity of the residuals was checked. Many of the data appear to have particularly heteroskedastic residuals. In many respects, homoscedasticity matters more than the normal distribution of the residuals. In Graphpad analyses if ANOVA is used but equal variances are assumed (when variances among groups are unequal then standard deviations assigned in each group will be wrong and thus incorrect p values are being calculated.

Based on the incomplete and/or wrong statistical analyses it is difficult to evaluate the study in greater depth.

While on the subject of stats, it is worth mentioning this misuse of statistics in Figure 3D, where the authors added the Slc34a1 transcript levels from controls in the correlation analyses, thereby driving the intercept down. Without the Control data there does not appear to be a correlation between the Slc34a1 levels and tumor size.

There is more. The authors make statements (e.g. in the figure levels as: "Correlations indicated by R2.". What does that mean? In a simple correlation, the P value is used to evaluate the strength of the slope being different from zero. The authors also give R2 values for the correlations but they do not provide R2 values for the other stats (like ANOVAs). Why not?

(2) The authors used antibodies for immunos and WBs. I checked those antibodies online and it was concerning:

(a) Many are discontinued.

(b) Many are not validated.

(c) Many performed poorly in the Immunos, e.g. FGF23, FGFR1, and Kotho are not really convincing. PO5F1 (gene: OCT4) is the one that looks convincing as it is expressed at the correct cell types.

(d) Others like NPT2A (product of gene SLC34A1) are equally unconvincing. Shouldn't the immuno show them to be in the plasma membrane?

If there is some brown staining, this does not mean the antibodies are working. If your antibodies are not validated then you ought to omit the immunos from the manuscript.

Reviewer #2 (Public Review):

Summary:

This study set out to examine microlithiasis associated with an increased risk of testicular germ cell tumors (TGCT). This reviewer considers this to be an excellent study. It raises questions regarding exactly how aberrant Sertoli cell function could induce osteogenic-like differentiation of germ cells but then all research should raise more questions than it answers.

Strengths:

Data showing the link between a disruption in testicular mineral (phosphate) homeostasis, FGF23 expression, and Sertoli cell dysfunction, are compelling.

Weaknesses:

Not sure I see any weaknesses here, as this study advances this area of inquiry and ends with a hypothesis for future testing.

La escritura creativa nos invita a explorar mundos imaginarios, conectar con nuestras emociones y reflexionar sobre el mundo que nos rodea es una herramienta poderosa para el desarrollo personal, la conexión con los demás y el cambio social me encantó mucho está tesis ya que nos comparte que mejora la comunicación, la expresión escrita, la creatividad y la inteligencia emocional fortalece la autoestima, aumenta confianza en uno mismo. Fomenta el pensamiento crítico, analizar y reflexionar sobre diferentes temas.

En resumen a todo este texto es que la escritura creativa es una herramienta valiosa para el desarrollo del alumno, tanto a nivel personal como académico. La escuela tiene la responsabilidad de fomentar la escritura creativa en el aula, proporcionando a los alumnos las herramientas y el apoyo necesarios para expresarse libremente a través de la escritura. Y así el niño pueda seguir progresando en todo el transcurso de su vida estudiantil.

Este texto me ha parecido muy interesaste pero lo que mas me gusto y me llamo la atención fue sobre la escritura creativa en el aula de Educación Primaria. Este trabajo no solo resalta la importancia de la creatividad en la enseñanza de la escritura, sino que también proporciona metodologías y propuestas didácticas concretas para implementar en el aula. Me ha gustado mucho la forma en que el trabajo combina la teoría con la práctica, proponiendo el uso de nuevas tecnologías, como blogs, para motivar a los estudiantes y desarrollar sus competencias lingüísticas. Además, la revisión del currículo y los métodos históricos de enseñanza de la escritura nos ha permitido conocer y comprender de una mejor manera la evolución de las prácticas educativas en este campo. En definitiva, considero que este trabajo es una valiosa herramienta para cualquier docente que busque fomentar la creatividad y mejorar las habilidades de escritura de sus alumnos ya que la escritura es vital para la expresión y comunicación de docentes a estudiantes y de estudiantes así los docentes.

Es tan cierto como escritores como Vargas Llosa (2001 nos hacen caer en cuenta en como nos hemos acostumbrado solo a escribir mensajes de texto en vez de volver ha escribir cartas en las cuales podemos expresarnos emociones y pensamiento los cuales son muy dificles de expresar o talvez en adentrarnos en leer llibros que nos puede hacer imaginar otras mundos y realidades, mandamos de un 1000000 de mensajes al dia pero no somos capaces de leer un libro escribir algo a mano es por eso que hoy en dia prefieren darle a un niño un celular en vez de un cuaderno o un libro esto causa muchos problemos debido a que genera falencias en el aparendizaje y concentración por que los niños se enfocan en lo artifical a pensar en otras cosas.

Se refiere a que debemos tener la disposición y la motivación para iniciar nuevas ideas, proyectos o acciones sin esperar a que otros te digan qué hacer. Implica ser proactivo y estar dispuesto a tomar la iniciativa para explorar nuevas posibilidades, experimentar con diferentes enfoques y buscar soluciones innovadoras.

Este texto nos menciona el que debemos incentivar la práctica de hablar, ya que así se mejora la claridad y precisión en la pronunciación de palabras y al igual a eso se aprende a apreciar y disfrutar los sonidos y ritmos de cada de las palabras que estamos aprendiendo.

Este texto menciona que el escribir es un acto de comunicación que debe ser planeado y por lo tanto antes de empezar a escribir, el escritor necesita pasar por una fase previa en la que organiza y estructura la información que quiere comunicar.

Este documento es muy interesante por que nos hace reflexionar y a su vez entender sobre la escritura en el aula de igual manera nos hacer ver como el ser humano es capaz de trasmitir emociones y sentimientos atravez de una escritura de hecho como es capaz de compartir sus pensamientos en una simple o compleja escritura es más si hoy en día lo replicaramos como en la antiguedad es más esta lectura nos caer en cuenta de tan importante que es fomentar la escritura creativa en los alumnos sobre todo nos ayuda a nosotros que vamos ha ser futuros maestros y as u vez nos reclaca lo negativo y positvo de las tecnologias o TICS en la educación pero a su expresando y proponiendo métodos efectivos para fomentar la escritura creatividad, partiendo de lo simple a lo complejo y permitiendo a los estudiantes escribir desde sus intereses pero sobre todo destacar que no debería ser por obligación sino por placer, por gusto por que les nace y les apasiona o como forma de expresar ,desahorgarse ante alguna situación .esto ayuda a cambiar el enfoque educativo hacia la creatividad e imaginación. El objetivo de nosotros como futuros docentes es transformar la educación y motivar a los estudiantes o alumn@s a disfrutar del proceso de escritura como una manera de desahogarse o expresar su vida no como una obligación por una nota si un simple placer por escribir y brindar información que para otros podria ser una salvación.

Acerca de este texto trata de decir que la escritura es considerada como una herramienta donde podemos expresar ideas, pensamientos, sentimientos o la información y debido esto es que nos podemos comunicar con otros. Debido a esto la escritura no debe ser vista únicamente como una actividad que se realiza por si misma, en tanto se puede decir que la escritura su principal objetivo es transmitir algo significativo y conectar con los demás.

Es tan real esto porque aveces solemos tomar un fracaso como un fin y no debe de ser asi de hecho los fracasos debe ser fomas de valentia para mejorar día a día de igual manera seria una oportunidad de seguir intentando algo hasta lograrlo esto nos ayuda a generar autoconfianza para no rendirnos sino para transformar los errores a aprendizajes para mejorar algo que se esta construyendo para así llegarlo a cumplir como una meta un logro de vida porque cada error tiene una enseñanza de vida.

La escritura es vital para la expresión y comunicación, pero muchos estudiantes son dejados al escribir en la escuela, el enfoque tradicional, centrado en memorizar reglas, no fomenta la creatividad, fomentar la escritura creativa desarrolla la invención y el pensamiento crítico, esenciales para el crecimiento personal ,los docentes necesitan recursos y metodologías, como blogs con estrategias prácticas, para enriquecer la experiencia de escritura en el aula también la escritura creativa es clave para formar comunicadores competentes, y es responsabilidad de los docentes hacerla significativa este seria mi comentario sobre el texto ya que lo que mas me llamo fue la creatividad en relación con la escritura y su importancia en esta.

El texto habla de la importancia de fomentar una escritura que vaya más allá de lo "formal", se habla de que la escritura debe ser libre para así provocar que los estudiantes generen ese gusto por escribir, que sean más imaginativos y creativos. Promover una escritura creativa.

yo creo que la escritura es fundamental para la comunicación human ya que nos permite no solo compartir ideas y conocimientos, sino también explorar y entender nuestras emociones compartirlas con alguien mas y hacer saber al resto como nos sentimos, a través de la escritura, podemos construir puentes con otros y dejar un legado que trasciende el tiempo ya que como nos dice esto jamás pasara de moda por que se a mantenido durante años, la escritura es un medio que nos ayuda a reflexionar y a conectar con el mundo.

La escritura creativa busca generar nuevas ideas, textos originales que pueden verse relacionadas con la poesía, la novela, el ensayo y otros textos que requieren de un pensamiento creativo.

La escritura tiene muchas funciones, la utilizamos en nuestro día al registrar direcciones, al hacer un resumen, al escribir un ensayo; al enviar un mensaje a alguien...Tiene demasiadas funciones que son esenciales en la sociedad actual y en toda la historia ya que prácticamente registra la historia.

En las ideas que plasma Álvarez, me doy cuenta de que la escritura creativa es un proceso artístico complejo que va más allá de la simple redacción. Reconozco que el desafío que implica transformar pensamientos y emociones abstractas en palabras concretas, especialmente ante la intimidante página en blanco. Me llamo mucho la atención que este acto de narración se considere un arte, ya que se eleva la escritura creativa a un nivel que trasciende la comunicación y abarca la expresión multidimensional en las ideas, sentimientos y experiencias personales.

Corrales (2001) explica que leer y escribir son habilidades importantes porque nos ayudan a entender el mundo y hablar sobre él, desde mi punto de vista esto es muy útil para mejorar nuestra escritura creativa, leer nos muestra diferentes formas de pensar y escribir, mientras que escribir nos permite expresar nuestras propias ideas sentimientos abriendo esa puerta para poder dar nuestra opinión o lo que nosotros creemos de algo, juntas, la lectura y la escritura nos ayudan a ser más creativos y pensar de manera crítica logrando que un día seamos los que con nuestra forma de pensar y expresarnos cambiemos el mundo en el que vivimos .

La creatividad es esencial para que los estudiantes vayan más allá de las expectativas y escriban textos que superan los estándares de la educación.

Este párrafo me intereso mucho ya que la importancia de su enfoque práctico en las Nuevas Tecnologías, considero que es acertado por su relevancia en el entorno actual del alumnado y su creciente presencia en el sistema educativo. Valoro positivamente esta consideración del contexto tecnológico de los estudiantes, ya que puede aumentar su interés y motivación. Sin embargo, tengo varias cuestiones sobre los desafíos que esta integración tecnológica puede suponer, como la formación del profesorado o la posible brecha digital entre estudiantes. A pesar de estos retos, veo en este enfoque una oportunidad para desarrollar formas de enseñanza y aprendizaje más dinámicas e interactivas, lo cual me parece una evolución necesaria en el ámbito educativo actual.

Estoy completamente de acuerdo con la afirmación esta afirmación, desarrollar el hábito de escribir regularmente es esencial para mejorar nuestras habilidades, la práctica constante nos permite encontrar nuestra voz y estilo, y cada texto es una oportunidad para aprender, hacer de la escritura un hábito diario es clave para perfeccionar este oficio.

Primacy effect下的中文例子似乎对应的是新奇效应。而新奇效应下的解释对应的是Primacy effect

Del texto que esta presente destaca como la escritura terapéutica como una herramienta poderosa para la expresión y comprensión emocional y explica cómo la escritura puede ser útil tanto en terapia como en el desarrollo personal. Además, menciona que escribir en días buenos puede proporcionar apoyo emocional en momentos difíciles la escritura no requiere habilidades literarias, sino una auténtica expresión de sentimientos.

Me identifico profundamente con esto. La idea de hablar cara a cara con un terapeuta puede ser un poco incomodo, expresar mis sentimientos verbalmente se vuelve casi imposible

Escribir una carta en un "día bueno" para ti mismo puede ser una herramienta poderosa. En momentos de debilidad leer palabras de apoyo y comprensión que vengan de ti mismo te ayudará a encontrar fuerza y ánimo cuando más lo necesites.

En la actualidad la mayoría de personas no encuentra formas de expresión y este método ayuda a muchos adolescentes y personas que no tengan forma de asistir a un terapeuta el texto tiene toda la razón porque va a ayudar a aquellas personas que no son capaces de expresarse a escribir sus sentimientos sus emociones mediante la escritura mediante un diario personal que les va a ayudar a sentirse mejor y sí es una muy buena terapia Y como dice ahí puede ser la más poderosa pienso aplicar este método para mí misma.

Para algunas personas, escribir es simplemente una acción para comunicarse pero para otras, la escritura es una herramienta poderosa para la comprensión emocional. Al escribir, pueden explorar sus pensamientos y sentimientos más profundos, organizar sus ideas y encontrar claridad en medio del caos emocional. Este proceso puede ser terapéutico y revelador, permitiendo a las personas conectarse con su yo interior de una manera que otras formas de expresión no pueden igualar.

Pues el texto tiene toda la razón ya que como lo menciona es súper importante que se exprese emocionalmente la persona que escribe y así logre una paz interior gracias a esta escritura terapéutica y me parece súper interesante que no tenga forma que no tenga parámetros para escribir que no sea basado en ningún reglamento sino en Cómo pensamos y en cómo nos expresamos cada una de las personas que elegimos escribir así para sanarnos emocionalmente.

Me parece muy interesante este método de utilizar la escritura terapéutica pienso que algunas personas no somos capaces de expresar nuestras emociones delante de alguien que nos quiera ayudar como un terapeuta pero si tal vez lo integramos como dice en el texto a utilizar esta escritura para ayudarnos a nosotros mismos y poder superar nuestras dificultades emocionales y también entender de un modo diferente las cosas y a las personas pienso que este método puede ayudar mucho a las futuras generaciones porque vivimos en un mundo rodeado de tecnología y es verdad que a veces no tenemos tiempo de agendar una cita con un terapeuta o a veces no nos animamos por miedo a decir que tal vez Estamos locos pero es una buena forma de ayudarnos a nosotros mismos y ayudar a las personas que nos rodean ya que si estamos nosotros mal emocionalmente también afectamos a las personas que también nos quieren implementar esta estrategia sería muy beneficioso en mi vida.

La escritura terapéutica es una herramienta poderosa que va más allá de ser solo un medio para el desarrollo personal y el bienestar emocional.

La escritura les brinda un espacio seguro y libre de juicios donde pueden plasmar sus pensamientos, emociones y experiencias de una manera que les resulte más accesible y confortable.

Como menciona el texto, se ha demostrado que la escritura terapéutica es eficaz en la recuperación de personas que enfrentan problemas de salud mental como la depresión o el trastorno de estrés postraumático, también es importante destacar que la escritura terapéutica puede ser especialmente beneficiosa para aquellas personas que encuentran dificultades para expresar sus sentimientos verbalmente, ya sea por ansiedad, angustia u otros motivos.

Este artículo trata sobre la escritura terapéutica y sus beneficios para la salud mental. Discute el uso de la escritura como herramienta para expresar emociones no expresadas o inexploradas. El autor describe el método del diario intensivo y otras formas de escritura expresiva. La escritura terapéutica puede ser útil para personas que sufren de depresión o trastorno de estrés postraumático. El artículo también menciona los beneficios de escribir cartas a uno mismo en los "días buenos" para leer en los "días malos".

Me parece muy bueno el método que se está utilizando en la actualidad de parte de los terapeutas al ofrecer sus servicios en línea a través del correo electrónico ya que la mayoría de personas no dispone del tiempo suficiente para ir presencialmente a una cita sin embargo este sistema puede proporcionar ciertas desventajas como por ejemplo: al estar comunicándose vía correo electrónico con el terapeuta donde a veces las personas no son capaces de expresar su situación emocional ni aun estando de una manera presencial con el terapeuta ni mucho menos por una plataforma virtual, evitando así al terapeuta obtener toda la información para poder ayudar.

quel est code html utilisé pour obtenir ceci ?

Mendelian randomization (commonly abbreviated to MR) is a method using measured variation in genes to examine the causal effect of an exposure on an outcome

Remove T

Change to new tool and new abbreviation August 1

Change to Data Management Planner

This page should be pitches as the main resource for finding secondary datasets, not an after thought.

The link in the bullet point will likely go dead from August 1 as the checklist will become part pf the planner. I think you can coner this later.

Oh I love this idea! I think hearing questions and concerns straight from the staff is a great idea. The teachers are able to get answers quickly and ask follow up questions if needed.

Open communication between all group is vital to make the school district a positive one.

When all of the issues are able to be settled before they get to individual schools then the school and teacher are able to provide students with their education. If school districts are able to focus on academics this will entice other families to come to the school district that strives in academics.

This danger zone statement is one that will tear a county apart. The teachers will stand together and ruin the school board.

Unfortunately I have seen where individuals forget this question. I feel certain individuals have their own plan without doing what is best for the child. We need to definitely start asking this question more.

If this is how the school board and superintendent act, this is only going to filter down to staff then to students then the community. This is going to cause a lot of issues for the entire community.

This is such a powerful statement! I feel as though this should be the mentality of everyone in education.

I think professional development to board members is great idea. I was just recently thinking the school board needs to be held responsible attending PD put on school board associattions.

Unfortunately about 5 years ago this was an issue for my school district. The board of education had some members siding with the superintendent and while others were not. This made for a very toxic environment.

Southern California welcomes the world’s first fully autonomous, AI-powered restaurant, CaliExpress by Flippy. Located in Pasadena, this innovative eatery showcases robots cooking burgers and fries from start to finish, offering customizable orders. Developed through a collaboration between Cali Group, Miso Robotics, and PopID, the restaurant aims to revolutionize dining with automated ordering and cooking processes. Promising reduced waste and enhanced efficiency, it marks a significant advancement in restaurant technology and operational sustainability. The venture highlights the future of dining experiences with minimal human intervention, setting a new standard in culinary automation.

artificialintelligence #restaurant #california #robots #technology

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What is this?

DOI: 10.1007/s00412-020-00732-x

Resource: (BDSC Cat# 8622,RRID:BDSC_8622)

Curator: @olekpark

SciCrunch record: RRID:BDSC_8622

What is this?

DOI: 10.1080/01677063.2019.1710144

Resource: RRID:BDSC_24743

Curator: @olekpark

SciCrunch record: RRID:BDSC_24743

What is this?

DOI: 10.1080/01677063.2019.1710144

Resource: RRID:BDSC_19491

Curator: @olekpark

SciCrunch record: RRID:BDSC_19491

What is this?

DOI: 10.1080/01677063.2019.1710144

Resource: BDSC_10847

Curator: @olekpark

SciCrunch record: RRID:BDSC_10847

What is this?

DOI: 10.3390/cells9020270

Resource: RRID:BDSC_60110

Curator: @olekpark

SciCrunch record: RRID:BDSC_60110

What is this?

DOI: 10.3390/cells9020270

Resource: RRID:BDSC_57426

Curator: @olekpark

SciCrunch record: RRID:BDSC_57426

What is this?

DOI: 10.3390/cells9020270

Resource: (BDSC Cat# 34021,RRID:BDSC_34021)

Curator: @olekpark

SciCrunch record: RRID:BDSC_34021

What is this?

DOI: 10.3390/cells9020270

Resource: (BDSC Cat# 31353,RRID:BDSC_31353)

Curator: @olekpark

SciCrunch record: RRID:BDSC_31353

What is this?

DOI: 10.3390/cells9020270

Resource: (BDSC Cat# 4274,RRID:BDSC_4274)

Curator: @olekpark

SciCrunch record: RRID:BDSC_4274

What is this?

DOI: 10.3390/cells9020270

Resource: RRID:BDSC_12212

Curator: @olekpark

SciCrunch record: RRID:BDSC_12212

What is this?

DOI: 10.3390/cells9020270

Resource: (BDSC Cat# 3605,RRID:BDSC_3605)

Curator: @olekpark

SciCrunch record: RRID:BDSC_3605

What is this?

DOI: 10.3390/cells9020270

Resource: BDSC_35695

Curator: @olekpark

SciCrunch record: RRID:BDSC_35695

What is this?

DOI: 10.3390/cells9020270

Resource: RRID:BDSC_43189

Curator: @olekpark

SciCrunch record: RRID:BDSC_43189

What is this?

DOI: 10.1371/journal.pgen.1008581

Resource: Bloomington Drosophila Stock Center (RRID:SCR_006457)

Curator: @olekpark

SciCrunch record: RRID:SCR_006457

What is this?

DOI: 10.1242/jeb.207407

Resource: BDSC_61771

Curator: @olekpark

SciCrunch record: RRID:BDSC_61771

What is this?

DOI: 10.1242/jeb.207407

Resource: (BDSC Cat# 9466,RRID:BDSC_9466)

Curator: @olekpark

SciCrunch record: RRID:BDSC_9466

What is this?

DOI: 10.1242/jeb.207407

Resource: (BDSC Cat# 5130,RRID:BDSC_5130)

Curator: @olekpark

SciCrunch record: RRID:BDSC_5130

What is this?

DOI: 10.1242/jeb.207407

Resource: BDSC_25869

Curator: @olekpark

SciCrunch record: RRID:BDSC_25869

What is this?

DOI: 10.1242/jeb.207407

Resource: RRID:BDSC_27494

Curator: @olekpark

SciCrunch record: RRID:BDSC_27494

What is this?

DOI: 10.1242/jeb.207407

Resource: (BDSC Cat# 36303,RRID:BDSC_36303)

Curator: @olekpark

SciCrunch record: RRID:BDSC_36303

What is this?

DOI: 10.1242/jeb.207407

Resource: BDSC_28333

Curator: @olekpark

SciCrunch record: RRID:BDSC_28333

What is this?

DOI: 10.1242/jeb.207407

Resource: (BDSC Cat# 458,RRID:BDSC_458)

Curator: @olekpark

SciCrunch record: RRID:BDSC_458

What is this?

DOI: 10.1242/jeb.207407

Resource: (BDSC Cat# 37516,RRID:BDSC_37516)

Curator: @olekpark

SciCrunch record: RRID:BDSC_37516

What is this?

DOI: 10.1242/jeb.207407

Resource: (BDSC Cat# 51981,RRID:BDSC_51981)

Curator: @olekpark

SciCrunch record: RRID:BDSC_51981

What is this?

DOI: 10.3324/haematol.2019.219394

Resource: (BDSC Cat# 8622,RRID:BDSC_8622)

Curator: @olekpark

SciCrunch record: RRID:BDSC_8622

What is this?

DOI: 10.3324/haematol.2019.219394

Resource: (BDSC Cat# 1104,RRID:BDSC_1104)

Curator: @olekpark

SciCrunch record: RRID:BDSC_1104

What is this?

DOI: 10.1534/g3.119.401034

Resource: BDSC_60388

Curator: @olekpark

SciCrunch record: RRID:BDSC_60388

What is this?

DOI: 10.1534/g3.119.401034

Resource: (BDSC Cat# 53347,RRID:BDSC_53347)

Curator: @olekpark

SciCrunch record: RRID:BDSC_53347

What is this?

DOI: 10.1534/g3.119.401034

Resource: RRID:BDSC_34821

Curator: @olekpark

SciCrunch record: RRID:BDSC_34821

What is this?

DOI: 10.1534/g3.119.401034

Resource: BDSC_33745

Curator: @olekpark

SciCrunch record: RRID:BDSC_33745

What is this?

DOI: 10.1534/g3.119.401034

Resource: RRID:BDSC_27502

Curator: @olekpark

SciCrunch record: RRID:BDSC_27502

What is this?

DOI: 10.1534/g3.119.401034

Resource: RRID:BDSC_38283

Curator: @olekpark

SciCrunch record: RRID:BDSC_38283

What is this?

DOI: 10.1534/g3.119.401034

Resource: RRID:BDSC_64041

Curator: @olekpark

SciCrunch record: RRID:BDSC_64041

What is this?

DOI: 10.1534/g3.119.401034

Resource: (BDSC Cat# 27035,RRID:BDSC_27035)

Curator: @olekpark

SciCrunch record: RRID:BDSC_27035

What is this?

DOI: 10.1534/g3.119.401034

Resource: BDSC_32891

Curator: @olekpark

SciCrunch record: RRID:BDSC_32891

What is this?

DOI: 10.1534/g3.119.401034

Resource: BDSC_33403

Curator: @olekpark

SciCrunch record: RRID:BDSC_33403

What is this?

DOI: 10.1534/g3.119.401034

Resource: (BDSC Cat# 25750,RRID:BDSC_25750)

Curator: @olekpark

SciCrunch record: RRID:BDSC_25750

What is this?

DOI: 10.1534/g3.119.401034

Resource: (BDSC Cat# 25756,RRID:BDSC_25756)

Curator: @olekpark

SciCrunch record: RRID:BDSC_25756

What is this?

DOI: 10.3389/fcell.2020.00032

Resource: (BDSC Cat# 64349,RRID:BDSC_64349)

Curator: @olekpark

SciCrunch record: RRID:BDSC_64349

What is this?

DOI: 10.1093/nar/gkaa072

Resource: Bloomington Drosophila Stock Center (RRID:SCR_006457)

Curator: @olekpark

SciCrunch record: RRID:SCR_006457

What is this?

DOI: 10.1083/jcb.201905091

Resource: (BDSC Cat# 35514,RRID:BDSC_35514)

Curator: @olekpark

SciCrunch record: RRID:BDSC_35514

What is this?

DOI: 10.1083/jcb.201905091

Resource: (BDSC Cat# 6839,RRID:BDSC_6839)

Curator: @olekpark

SciCrunch record: RRID:BDSC_6839

What is this?

DOI: 10.1083/jcb.201905091

Resource: (BDSC Cat# 1509,RRID:BDSC_1509)

Curator: @olekpark

SciCrunch record: RRID:BDSC_1509

What is this?

DOI: 10.1083/jcb.201905091

Resource: BDSC_28719

Curator: @olekpark

SciCrunch record: RRID:BDSC_28719

What is this?

DOI: 10.1083/jcb.201905091

Resource: RRID:BDSC_38305

Curator: @olekpark

SciCrunch record: RRID:BDSC_38305

What is this?

DOI: 10.1083/jcb.201905091

Resource: RRID:BDSC_28531

Curator: @olekpark

SciCrunch record: RRID:BDSC_28531

What is this?

DOI: 10.1083/jcb.201905091

Resource: RRID:BDSC_58208

Curator: @olekpark

SciCrunch record: RRID:BDSC_58208

What is this?

DOI: 10.1083/jcb.201905091

Resource: BDSC_31470

Curator: @olekpark

SciCrunch record: RRID:BDSC_31470

What is this?

DOI: 10.1083/jcb.201905091

Resource: BDSC_31666

Curator: @olekpark

SciCrunch record: RRID:BDSC_31666

What is this?

DOI: 10.1083/jcb.201905091

Resource: BDSC_50515

Curator: @olekpark

SciCrunch record: RRID:BDSC_50515

What is this?

DOI: 10.1083/jcb.201905091

Resource: BDSC_29587

Curator: @olekpark

SciCrunch record: RRID:BDSC_29587

What is this?

DOI: 10.1083/jcb.201905091

Resource: RRID:BDSC_53331

Curator: @olekpark

SciCrunch record: RRID:BDSC_53331

What is this?

DOI: 10.1083/jcb.201905091

Resource: RRID:BDSC_36736

Curator: @olekpark

SciCrunch record: RRID:BDSC_36736

What is this?

DOI: 10.1083/jcb.201905091

Resource: (BDSC Cat# 25862,RRID:BDSC_25862)

Curator: @olekpark

SciCrunch record: RRID:BDSC_25862

What is this?

DOI: 10.1083/jcb.201905091

Resource: RRID:BDSC_38234

Curator: @olekpark

SciCrunch record: RRID:BDSC_38234

What is this?

DOI: 10.1083/jcb.201905091

Resource: BDSC_34377

Curator: @olekpark

SciCrunch record: RRID:BDSC_34377

What is this?

DOI: 10.1083/jcb.201905091

Resource: BDSC_26708

Curator: @olekpark

SciCrunch record: RRID:BDSC_26708

What is this?

DOI: 10.1083/jcb.201905091

Resource: RRID:BDSC_12425

Curator: @olekpark

SciCrunch record: RRID:BDSC_12425

What is this?

DOI: 10.1083/jcb.201905091

Resource: (BDSC Cat# 7376,RRID:BDSC_7376)

Curator: @olekpark

SciCrunch record: RRID:BDSC_7376

What is this?

DOI: 10.1083/jcb.201905091

Resource: BDSC_23561

Curator: @olekpark

SciCrunch record: RRID:BDSC_23561

What is this?

DOI: 10.1242/dev.184390

Resource: (BDSC Cat# 51664,RRID:BDSC_51664)

Curator: @olekpark

SciCrunch record: RRID:BDSC_51664

What is this?

DOI: 10.1242/dev.184390

Resource: (BDSC Cat# 42704,RRID:BDSC_42704)

Curator: @olekpark

SciCrunch record: RRID:BDSC_42704

What is this?

DOI: 10.1242/dev.184390

Resource: (BDSC Cat# 35045,RRID:BDSC_35045)

Curator: @olekpark

SciCrunch record: RRID:BDSC_35045

What is this?

DOI: 10.1242/dev.184390

Resource: BDSC_63004

Curator: @olekpark

SciCrunch record: RRID:BDSC_63004

What is this?

DOI: 10.1073/pnas.1909814117

Resource: (BDSC Cat# 34747,RRID:BDSC_34747)

Curator: @olekpark

SciCrunch record: RRID:BDSC_34747

What is this?

DOI: 10.1073/pnas.1909814117

Resource: (BDSC Cat# 2077,RRID:BDSC_2077)

Curator: @olekpark

SciCrunch record: RRID:BDSC_2077

What is this?

DOI: 10.1073/pnas.1909814117

Resource: (BDSC Cat# 8848,RRID:BDSC_8848)

Curator: @olekpark

SciCrunch record: RRID:BDSC_8848

What is this?

DOI: 10.1073/pnas.1909814117

Resource: (BDSC Cat# 27390,RRID:BDSC_27390)

Curator: @olekpark

SciCrunch record: RRID:BDSC_27390

What is this?

DOI: 10.1016/j.celrep.2020.02.053

Resource: Bloomington Drosophila Stock Center (RRID:SCR_006457)

Curator: @olekpark

SciCrunch record: RRID:SCR_006457

What is this?