High impact information on tbx16

• Genetic screens in zebrafish have identified mutants with defects that disrupt specific stages of hematopoiesis and vasculogenesis, including the cloche, spadetail (tbx16), moonshine (tif1g), bloodless, and vlad tepes (gata1) mutants [1].
• Consistent with a common effect of dsRNA, regardless of sequence, injection of dsRNA from the lacZ gene was likewise effective in strongly reducing tbx16/spt and beta catenin mRNA in the blastula [2].
• These studies demonstrate that the molecular mechanisms that regulate hematopoiesis and vasculogenesis have been conserved throughout vertebrate evolution and the clo and spt genes are key regulators of these programs [3].
• In spt- embryos, par1 expression is both delayed and severely reduced whereas in flh- embryos, ectopic transcripts are detected in axial mesoderm [4].
• Analysis of gta3 expression in dorsalised embryos and in cyc and spt mutant embryos indicates that the neural expression of the gene is subject to control by signals from the mesoderm, including both the notochord and the somites, which influence the segmental organisation of expression in the spinal cord [5].

Biological context of tbx16

• We compared the effects of injecting dsRNA from the zebrafish tbx16/spadetail, nieuwkoid/bozozok, and Brachyury/no tail genes with dsRNA from the bacterial lacZ gene [2].
• The human genome does not appear to possess orthologues of zebrafish tbx6 or tbx16/spadetail [6].

Other interactions of tbx16

• We report on a new zebrafish T-box-containing gene, tbx16 [7].

References