Person: Manceau, Marie
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Manceau
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Marie
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Manceau, Marie
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Publication The Developmental Role of Agouti in Color Pattern Evolution(American Association for the Advancement of Science (AAAS), 2011) Manceau, Marie; Domingues, Vera S.; Mallarino, Ricardo; Hoekstra, HopiAnimal color patterns can affect fitness in the wild; however, little is known about the mechanisms that control their formation and subsequent evolution. We took advantage of two locally camouflaged populations of Peromyscus mice to show that the negative regulator of adult pigmentation, Agouti, also plays a key developmental role in color pattern evolution. Genetic and functional analyses showed that ventral-specific embryonic expression of Agouti establishes a prepattern by delaying the terminal differentiation of ventral melanocytes. Moreover, a skin-specific increase in both the level and spatial domain of Agouti expression prevents melanocyte maturation in a regionalized manner, resulting in a novel and adaptive color pattern. Thus, natural selection favors late-acting, tissue-specific changes in embryonic Agouti expression to produce large changes in adult color pattern.Publication Turing patterns: how the fish got its spots(Wiley-Blackwell, 2011) Metz, Hillery Claire; Manceau, Marie; Hoekstra, HopiPublication Convergence in pigmentation at multiple levels: mutations, genes and function(The Royal Society, 2010) Manceau, Marie; Domingues, V. S.; Linnen, Catherine; Rosenblum, E. B.; Hoekstra, HopiConvergence—the independent evolution of the same trait by two or more taxa—has long been of interest to evolutionary biologists, but only recently has the molecular basis of phenotypic convergence been identified. Here, we highlight studies of rapid evolution of cryptic coloration in vertebrates to demonstrate that phenotypic convergence can occur at multiple levels: mutations, genes and gene function. We first show that different genes can be responsible for convergent phenotypes even among closely related populations, for example, in the pale beach mice inhabiting Florida's Gulf and Atlantic coasts. By contrast, the exact same mutation can create similar phenotypes in distantly related species such as mice and mammoths. Next, we show that different mutations in the same gene need not be functionally equivalent to produce similar phenotypes. For example, separate mutations produce divergent protein function but convergent pale coloration in two lizard species. Similarly, mutations that alter the expression of a gene in different ways can, nevertheless, result in similar phenotypes, as demonstrated by sister species of deer mice. Together these studies underscore the importance of identifying not only the genes, but also the precise mutations and their effects on protein function, that contribute to adaptation and highlight how convergence can occur at different genetic levels.Publication Developmental mechanisms of stripe patterns in rodents(Springer Nature, 2016) Mallarino, Ricardo; Henegar, Corneliu; Mirasierra, Mercedes; Manceau, Marie; Schradin, Carsten; Vallejo, Mario; Beronja, Slobodan; Barsh, Gregory S.; Hoekstra, HopiMammalian color patterns are among the most recognizable characters found in nature and can have a profound impact on fitness. However, little is known about the mechanisms underlying their formation and subsequent evolution. Here we show that, in the African striped mouse (Rhabdomys pumilio), periodic dorsal stripes result from underlying differences in melanocyte maturation, which give rise to spatial variation in 6hair color,and we identify the transcription factor Alx3 as a regulator of this process.In 7embryonic dorsal skin, patterned expression of Alx3 foreshadows pigment stripes and acts 8to directly repress Mitf, a master regulator of melanocyte differentiation, giving rise to 9light-colored hair. Moreover, Alx3 is also upregulated in the light stripes of chipmunks, 10which have independently evolved a similar dorsal pattern.Our results reveal a 11previously unappreciated mechanism for modulating spatial variation in hair color and provide new insight into the ways in which phenotypic novelty evolves.Publication Melanism in Peromyscus Is Caused by Independent Mutations in Agouti(Public Library of Science, 2009) Kingsley, Evan; Manceau, Marie; Wiley, Christopher D.; Hoekstra, HopiIdentifying the molecular basis of phenotypes that have evolved independently can provide insight into the ways genetic and developmental constraints influence the maintenance of phenotypic diversity. Melanic (darkly pigmented) phenotypes in mammals provide a potent system in which to study the genetic basis of naturally occurring mutant phenotypes because melanism occurs in many mammals, and the mammalian pigmentation pathway is well understood. Spontaneous alleles of a few key pigmentation loci are known to cause melanism in domestic or laboratory populations of mammals, but in natural populations, mutations at one gene, the melanocortin-1 receptor (Mc1r), have been implicated in the vast majority of cases, possibly due to its minimal pleiotropic effects. To investigate whether mutations in this or other genes cause melanism in the wild, we investigated the genetic basis of melanism in the rodent genus Peromyscus, in which melanic mice have been reported in several populations. We focused on two genes known to cause melanism in other taxa, Mc1r and its antagonist, the agouti signaling protein (Agouti). While variation in the Mc1r coding region does not correlate with melanism in any population, in a New Hampshire population, we find that a 125-kb deletion, which includes the upstream regulatory region and exons 1 and 2 of Agouti, results in a loss of Agouti expression and is perfectly associated with melanic color. In a second population from Alaska, we find that a premature stop codon in exon 3 of Agouti is associated with a similar melanic phenotype. These results show that melanism has evolved independently in these populations through mutations in the same gene, and suggest that melanism produced by mutations in genes other than Mc1r may be more common than previously thought.