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Anterograde melanosome transport is essential for adaptive skin tanning response. However, the molecular components involved, their interplay, and regulation by external cues in melanosome transport remain under-explored. Silencing of kinesin motors revealed that several members including the established KIF5B and a novel candidate KIF1B, mediate melanosome movement. The camouflage behavior of zebrafish embryos induced by incident light or α-MSH requires kif1b, suggesting a conserved melanosome transport machinery across vertebrates. Interestingly, the peri-nuclear melanosome accumulation upon kinesin knockdown is recapitulated by the silencing of autophagy effector MAP1LC3B (LC3B). Pull-down assays identified KIF1B, but not KIF5B, to be the LC3B- associated kinesin. LC3B binds the adapter SKIP via its LIR docking region that is proximal to Thr12 residue, a site for phosphorylation by Protein Kinase A. We demonstrate that phosphorylation of LC3B at Thr12 is stimulated by α-MSH, which potentiates the anterograde melanosome transport. Thereby, our study identifies a novel kinesin motor KIF1B for melanosome movement and establishes LC3B as the key molecular component that facilitates α-MSH responsive mobilization of melanosomes.
Anterograde melanosome transport is essential for adaptive skin tanning response. However, the molecular components involved, their interplay, and regulation by external cues in melanosome transport remain under-explored. Silencing of kinesin motors revealed that several members including the established KIF5B and a novel candidate KIF1B, mediate melanosome movement. The camouflage behavior of zebrafish embryos induced by incident light or α-MSH requires kif1b, suggesting a conserved melanosome transport machinery across vertebrates. Interestingly, the peri-nuclear melanosome accumulation upon kinesin knockdown is recapitulated by the silencing of autophagy effector MAP1LC3B (LC3B). Pull-down assays identified KIF1B, but not KIF5B, to be the LC3B- associated kinesin. LC3B binds the adapter SKIP via its LIR docking region that is proximal to Thr12 residue, a site for phosphorylation by Protein Kinase A. We demonstrate that phosphorylation of LC3B at Thr12 is stimulated by α-MSH, which potentiates the anterograde melanosome transport. Thereby, our study identifies a novel kinesin motor KIF1B for melanosome movement and establishes LC3B as the key molecular component that facilitates α-MSH responsive mobilization of melanosomes.
Vertebrate craniofacial morphogenesis is a highly orchestrated process that is directed by evolutionarily conserved developmental pathways. Within species, canalized developmental programs typically produce only modest morphological variation. However, as a result of millennia of artificial selection, the domestic pigeon (Columba livia) displays radical variation in craniofacial morphology within a single species. One of the most striking cases of pigeon craniofacial variation is the short beak phenotype, which has been selected in numerous breeds. Classical genetic experiments suggest that pigeon beak length is regulated by a small number of genetic factors, one of which is sex-linked (Ku2 locus). However, the molecular genetic underpinnings of pigeon craniofacial variation remain unknown. To determine the genetic basis of the short beak phenotype, we used geometric morphometrics and quantitative trait loci (QTL) mapping on an F2 intercross between a short-beaked Old German Owl (OGO) and a medium-beaked Racing Homer (RH). We identified a single locus on the Z-chromosome that explains a majority of the variation in beak morphology in the RH x OGO F2 population. In complementary comparative genomic analyses, we found that the same locus is also strongly differentiated between breeds with short and medium beaks. Within the differentiated Ku2 locus, we identified an amino acid substitution in the non-canonical Wnt receptor ROR2 as a putative regulator of pigeon beak length. The non-canonical Wnt (planar cell polarity) pathway serves critical roles in vertebrate neural crest cell migration and craniofacial morphogenesis. In humans, homozygous ROR2 mutations cause autosomal recessive Robinow syndrome, a rare congenital disorder characterized by skeletal abnormalities, including a widened and shortened facial skeleton. Our results illustrate how the extraordinary craniofacial variation among pigeons can reveal genetic regulators of vertebrate craniofacial diversity.
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