Abstract
Hox genes and tail formation. Approached through global analysis of intraspecific evolutionary variants and targeted gain-of-function studies.
This fourth lesson begins with a brief reminder of some key points developed in the previous lesson, concerning in particular the study of a recent publication that addresses the question of tail length evolution, approaching it at the level of mouse populations evolving in different habitats, and using the tools of quantitative genetics that make it possible to isolate quantitative trait loci (QTL). In the system under discussion (different ecotypes of the silvestre mouse peromyscus maniculatus), no fewer than six different quantitative loci are involved in tail length variations. A potential candidate gene is Hoxd13, whose mRNA quantity seems to decrease in animals showing longer tails. Hypotheses are discussed to explain how this gene might act on this reduction, the most likely being an increase in the population of progenitor cells present in the tail bud, enabling greater lengthening.
This quantitative effect of the Hoxd13gene is reinforced by the analysis of previous studies which showed that when these Hox13 genes are expressed too early and too anteriorly (gain of function), the opposite phenotype was obtained, namely a reduction, or even significant truncation of the tail. The end of this lesson is devoted to the mechanisms of vertebra formation and number, returning to the initial question of the lecture, namely how DNA can modify structures during evolution, and the relationship between this genetic " coding " system (our genome) and the appearance of forms.
