10,000 Matching Annotations
  1. Jul 2025
    1. t5+1 could assemble these into αβ+ and γδε+ fragments, guided only by partially overlapping ‘−’ strands (Figure 6b, Figure 6—figure supplement 1). Through non-covalent association (Vaish et al., 2003; Mutschler et al., 2015), the ribozyme-synthesised αβ+ and γδε+ fragments spontaneously reconstituted a new catalytically active triplet polymerase ribozyme (with in vitro transcribed type 1 RNA)

      The ribozyme can build copies of parts of itself and put them together like puzzle pieces to regenerate function. That’s basically modular self-replication, which I thought only synthetic biology was capable of.

    2. RNA catalysis is dependent upon RNA folding, and this yields structures that can block replication of such RNAs. To address this apparent paradox, we have re-examined the building blocks used for RNA replication.

      This blew my mind, RNA has to fold into specific shapes to work like a ribozyme, but those same shapes make it harder to copy. It’s like building a key that locks itself.

    3. Although still inefficient, the fact that the nascent activity of the 0core ribozyme could already copy templates that had confounded an established RPR encouraged us to continue to seek improved triplet polymerase ribozymes to leverage this substrate behaviour.

      This early success gave the researchers a good reason to keep pushing forward, since it hinted that triplet-based RNA replication might help overcome a key obstacle in the field.

    4. he strong inhibitory role of this central feature of RNA leads to an antagonism between the degree to which an RNA sequence is able to fold into a defined three-dimensional structure to encode function (such as catalysis) and the ease with which it can be replicated (Boza et al., 2014).

      This "structure vs. replication" tradeoff is a bigger deal because it may have made it harder for life to get started using RNA as both the genetic material and the machinery for replication.

    5. Yet, although ribozymes can be made to copy straight RNA templates this way, folded RNA templates – including the replicase ribozyme itself – impede copying. In this apparent paradox, a ribozyme needs to fold to copy RNA, but when folded, is itself copied poorly. Here, Attwater et al. wondered if choosing different building blocks might overcome this contradiction.

      I think this presents a contradiction, that the structure hat enables function also hinders duplication. However, the sentence introduces a key barrier that the research seeks to address.

    6. RNA oligonucleotides

      This is short, synthetic strands of RNA, typically ranging from 2 to 50 nucleotides in length, used in various molecular biology applications

    7. template secondary structures.

      This is the folded conformations that a DNA or RNA template can adopt due to intramolecular base pairing, forming structures like hairpins or stem-loops, It can interrupt or intervene with DNA replication, transcription, translation and etc.

    8. no replicase ribozyme has been observed in existing life forms;

      Most likely because they have been replaced by more efficient protein enzymes due to evolution.

    1. These observations suggest that the pleiotropic effects of yellow on male mating success might result from effects of yellow in the adult CNS, particularly in fru-expressing neurons.

      This sentence really shows how complex and interconnected gene function can be. It's not just that the yellow gene affects pigmentation, it might also influence behavior through its role in specific brain cells.

    2. It seemed worthwhile therefore to examine more closely one example of a gene mutation affecting behavior and to ask two questions, (1) how does it bring about its effect? [and], (2) what part might it play in evolution?”

      Even back in 1956, Bastock was asking questions that are still relevant today, not just about how a gene affects behavior, but also what that means in terms of evolution.

    3. The study reveals the importance of scientists considering that genes that affect behavior may do so by changing anatomy rather than by altering the brain

      This is a reminder to scientists (and us) that behavior isn’t just about brain chemistry; sometimes it’s about how the body is built.

    4. Yellow protein is expressed in sex combs (Hinaux et al., 2018, Figure 3G,H), where it is presumably required for synthesis of black dopamine melanin in the sex comb ‘teeth’.

      Melanization = adding dark pigment (melanin) to certain body parts. In this case, melanization makes the sex combs stronger and more rigid, helping males grab females. Without yellow, the sex combs are lighter and weaker.

    5. t expression of yellow in fru-expressing cells is neither necessary nor sufficient for yellow’s effect on male mating success.

      Yellow doesn’t need to be in brain cells to affect mating; the problem is somewhere else.

    6. The yellow males lack melanin pigments in their sex combs, which changes their structure.

      Key shift from neural to anatomical explanation, behavioral defect actually caused by structural changes in sex combs, not brain chemistry.

    7. However, we found that suppressing yellow expression in the larval CNS, dopaminergic neurons, or serotonergic neurons (Figure 2—figure supplement 3, FET, P values ranging from 0.45 to 1), or in all neurons (Figure 2E, FET, p=1 in all cases) or all glia (Figure 2F, FET, p=1), had no significant effect on male mating success.

      This result was surprising because it shows that turning off yellow in key parts of the nervous system—including neurons involved in mood and movement—does not affect male mating behavior. This suggests that yellow doesn’t act in the brain or nerves to influence mating, challenging the original hypothesis.