Non-homologous genes, homologous morphology
A growing number of cases demonstrate that the inverse situation, where genes that are not homologous encode a homologous morphological feature, can also occur. One of the first cases to be recognized involves evolutionary changes in the developmental roles of even-skipped (eve), which encodes a homeodomain transcription factor...
http://biology.mcgill.ca/faculty/abouheif/articles/Wray, Abouheif 1998.pdf
Alright, let's take a look:
"homologous structures (segments) are present but at least one homologous gene no longer contributes to their development"
What this paper is talking about is a complex development of a body plan controlled by numerous genes that no longer uses one of those genes, yet the overall structure still develops due to the remaining genes.
Now, lets read a bit more on that
eve gene as I'm a few years removed from my entomology training:
http://www.sdbonline.org/sites/fly/segment/evenskp1.htm
"One of EVE's primary functions is regulation of segment polarity through EVE's indirect regulation of
engrailed. In odd parasegments, graded expression of
eve establishes the
en stripes by setting the boundaries of the activator
paired and the repressors
runt and
sloppy paired (Fujioka, 1995). Expression of
en in even parasegments results from activation by Fushi tarazu (with Ftz-f1 as a cofactor). Only the most anterior cells of each
ftz stripe express
en and this restriction is dependent upon
odd-skipped and
naked."
And hold on again, getting called away. I'll finish the post later, but that should start laying the groundwork for some of the trouble with your position.
And back.
Let's also look at a rundown of insect segmentation generally:
http://what-when-how.com/insects/segmentation-insects/
I know, a generalized explain-stuff website isn't the most robust source, but it's the most clearly written rundown I was able to locate quickly and user friendliness is probably good in this discussion. If you feel prepared to tackle denser writing, i can provide a more comprehensive link.
Anyway, this breaks down the phases of segmentation:
The Gap Genes
The gap genes are so named because mutations in this class of genes cause deletions of several contiguous segments causing a “gap” in the resulting larva. The gap genes read the informational gradients set up by the maternal genes and along with cross-regulatory inputs from other gap genes, become expressed in broad but well-defined domains across the early embryo that roughly correspond to the regions that are deleted in the mutants. All of the gap genes encode transcription factors that act together to regulate expression of the downstream pair-rule genes.
The Pair-Rule Genes
The expression and function of the pair-rule genes reveals the first periodic patterns in the Drosophila embryo. Like the gap genes, the pair-rule class of genes was originally defined through their loss of function phenotypes—in this case, deletions with a two-segment periodicity. Accordingly, most of the pair-rule genes go through a phase of expression consisting of seven stripes—corresponding to a two-segment periodicity—beginning at the syncitial blastoderm stage of the embryo and persisting through cellularization. When the striped pattern for one such pair-rule gene, even-skipped . was first observed, it was thought that the beautiful regularity of the pattern was due to some sort of chemical oscillation that could be modeled with reaction-diffusion equations. Instead, it turns out that stripes are specified individually by the upstream gap and maternal genes acting directly on the DNA regulatory regions that control even-skipped expression. The pair-rule genes encode transcription factors that work together to regulate the final level of the segmentation hierarchy, the segment polarity genes.
The Segment Polarity Genes
The segment polarity genes were also originally identified in genetic screens and named for their mutant phenotypes, which show defects in every segment. These genes are generally expressed in patterns of segmental stripes and include not just transcription factors, but also various receptors, ligands, and enzymes that are used in cell-cell communication, and act to maintain and further refine the pattern of segments that has been elaborated.
The Homeotic Genes
A final category of genes, the homeotic genes, do not act to produce segments, but rather give identity to the segments. Mutations in these genes result in the transformation of one or more segments to the identity of another segment. For example, certain loss of function mutations in proboscipedia cause legs to appear in the place of the adult labial palps. The homeotic genes are primarily regulated by the gap genes, although pair-rule and segment polarity genes also have an important role in defining the precise boundaries of homeotic gene expression. All the homeotic genes encode a family of closely related transcription factors and, in Drosophila, are organized into two complexes on one of the chromosomes. Interestingly, the expression of the home-otic genes along the body axis and their arrangement in the genome are roughly co-linear; homeotic genes expressed in anterior segments of the embryo are situated 3 . in the complex, while genes expressed in the posterior are 5 . in the complex. This co-linear arrangement is highly conserved throughout the bilaterian animals, but the reasons for this chromosomal arrangement are not fully understood.
Now, you'll notice that pair rule signaling isn't the first group of genes involved. it kicks in after the Gap genes.
It also gets into some of the different mechanisms for controlling segment formation, which might be interesting to dig into to determine if
eve is utilized in all forms, or could be a late arrival to this party.
I hope we can agree that one gene that helps regulation of one specific part of segmentation no longer having that role is VERY different than a homologous structure that does not share homologous genes with other organisms with those homologous structures generally.
Now, there is something interesting I noticed. The paper states that
eve is part of the pair rule group of genes rather than segment polarity as my link states. This could be a slightly different use in fruit flies, which my link was discussing specifically, but if someone here is better with entomology than me, I'd love to get some more info on it.
I'm going on way too long, so I'll stop here.
![[serious]](/data/avatars/m/160/160873.jpg?1431539545){kind=avatar}
I am impressed. It is not very often that someone will admit when they are wrong. I find it refreshing.
