High impact information on snai1a

• Together these data suggest that Nrz, in addition to its effect on apoptosis, contributes to cell movements during gastrulation by negatively regulating the expression of Snail-1, a transcription factor that controls cell adhesion [1].
• This was not caused by the absence of neural crest cells or their impaired migration into the pharyngeal arches, as shown by expression of dlx2 and snail1, but by the inability of these cells to differentiate into chondroblasts [2].
• Skeletal stainings and the expression pattern of myoD and snail1 suggest that anteroposterior patterning within individual somites is abnormal [3].
• Later, sna-1 is expressed in neural crest and mesodermal derivatives of the head region [4].
• Maternal and zygotic sna-1 transcripts are ubiquitously distributed in zebrafish embryos of cleavage and blastula stages [4].

Biological context of snai1a

• Transcripts of a newly discovered gene called snail2, encoding a zinc finger protein of the Snail family, first appear in rows of cephalic mesendodermal cells in gastrulating zebrafish embryos [5].

Anatomical context of snai1a

• In situ hybridization shows that the quantity of snail1 RNA increases at the margin of the blastoderm in cells that involute during gastrulation [6].
• In addition, earlier during development, in the zebrafish gastrula, nrz knockdown results in an increase of snail-1 expression at the margin and frequent gastrulation arrest at the shield stage, independently of apoptosis [1].
• As gastrulation begins, snail1 RNA disappears from the dorsal axial mesoderm and becomes restricted to the paraxial mesoderm and the tail bud. snail1 RNA increases in cells that define the posterior border of each somite and then disappears when somitic cells differentiate [6].

References