We then evolved the deletion strain and observed that the genetic adaptation was recurrently based on a strategic mutation that changed the anticodon of other tRNA genes to match that of the deleted one.
This is a key finding. It highlights how a single point mutation in an anticodon can functionally replace a lost tRNA, emphasizing the adaptability of the translational machinery.
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.
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.
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.
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.
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.
Approximately 65% of human disease genes are estimated to have counterparts in D. melanogaster
This demonstrates the genetic similarity between D. melanogaster and humans, reinforcing its value as a model organism for studying human disease mechanisms.
Few studies of D. melanogaster have been done in the wild, but those that have reveal a different picture of wild flies.
This highlights the research gap between laboratory and field studies. Understanding wild populations is important to get a complete picture of the species' biology and evolution.