Sdf1a patterns zebrafish melanophores and links the somite and melanophore pattern defects inchokermutants

Abstract

Pigment pattern formation in zebrafish presents a tractable model system for studying the morphogenesis of neural crest derivatives. Embryos mutant for choker manifest a unique pigment pattern phenotype that combines a loss of lateral stripe melanophores with an ectopic melanophore 'collar' at the head-trunk border. We find that defects in neural crest migration are largely restricted to the lateral migration pathway, affecting both xanthophores (lost) and melanophores (gained) in choker mutants. Double mutant and timelapse analyses demonstrate that these defects are likely to be driven independently, the collar being formed by invasion of melanophores from the dorsal and ventral stripes. Using tissue transplantation, we show that melanophore patterning depends upon the underlying somitic cells, the myotomal derivatives of which -both slow-and fast-twitch muscle fibres -are themselves significantly disorganised in the region of the ectopic collar. In addition, we uncover an aberrant pattern of expression of the gene encoding the chemokine Sdf1a in choker mutant homozygotes that correlates with each aspect of the melanophore pattern defect. Using morpholino knock-down and ectopic expression experiments, we provide evidence to suggest that Sdf1a drives melanophore invasion in the choker mutant collar and normally plays an essential role in patterning the lateral stripe. We thus identify Sdf1 as a key molecule in pigment pattern formation, adding to the growing inventory of its roles in embryonic development.

Mechanisms driving neural crest induction and migration in the zebrafish andXenopus laevis

“…234 In the zebrafish, Sdf1a signaling has been implicated in melanophore patterning; melanocytes are attracted to the site of the implantation of an sdf1 coated bead. 236 There are two cxcr4 genes in zebrafish, cxcr4a and cxcr4b; only cxcr4a is expressed within neural crest cells. 237 Loss of Cxcr4a, but not Cxcr7b, results in aberrant cranial neural crest cell migration in the anterior stream, resulting in neurocranial defects and cranial ganglia dismorphogenesis.…”

Quadruple zebrafish mutant reveals different roles of Mesp genes in somite segmentation between mouse and zebrafish

“…Expression of cxcl12a in the superficial horizontal myoseptum was reported to have important roles in the pattern formation of various tissues and cells in the body surface, including migration of the posterior lateral line ( pLL) primordium and distribution of pigment cells at the body surface (David et al, 2002;Svetic et al, 2007). In the wild-type embryo, neuromasts, which are repetitively deposited from the pLL primordium during its migration, were aligned along the A-P body axis in the trunk and tail (Fig.…”

“…7B). Disrupted expression of cxcl12a in the superficial horizontal myoseptum was reported to affect neural crest migration along the lateral pathway in meox1 (choker) mutants, resulting in a disturbed pattern of pigment cells (Svetic et al, 2007). Thus, expression of this chemokine ligand in the medial surface of somites is required for proper alignment of pigment cells in medial body surface region.…”

Modular development of the teleost trunk along the dorsoventral axis and zic1/zic4 as selector genes in the dorsal module

“…As ectodermal organs develop at specific times and in distinct regions of the trunk, the mechanism of mesodermal-ectodermal interaction could differ depending on an organ. Melanophores are known to be attracted by the chemokine Sdf1 (Svetic et al, 2007), which might be secreted from the dorsalmost and ventralmost somites to establish the dorsal and ventral melanophore alignments. The size of the dorsal finfold in zebrafish can be modified by perturbing FGF signaling (Abe et al, 2007).…”