Wang Han, Lee Eric Myung-Jae, Sperber Steven M, Lin Shuo, Ekker Marc, Long Qiaoming
Department of Zoology and Stephenson Research and Technology Center, University of Oklahoma, Norman, OK 73019, USA.
Gene Expr Patterns. 2007 Jan;7(3):318-22. doi: 10.1016/j.modgep.2006.08.004. Epub 2006 Aug 26.
We report the expression patterns of tsh1, a zebrafish homologue of the Drosophila homeotic gene teashirt. Expression of tsh1 is first detected at the 2-somite stage (10h post-fertilization, hpf) at the anterior end of the spinal cord. Expression expands toward the posterior spinal cord, and by the prim-5 stage (24 hpf) tsh1 transcripts are detected throughout spinal cord. Between the 14- and 25-somite stage (16-24 hpf), spinal cord expression shows a clear anterior boundary at the rostral margin of rhombomere 7. Around the prim-25 stage (36 hpf), while the spinal expression of tsh1 decreases, new expression is detected in the pectoral fin buds and dorsal forebrain. By the long-pec stage (48 hpf), spinal cord expression is undetectable, but strong expression is observed in the rhombencephalon, telencephalon, tectum opticum, midbrain-hindbrain boundary, in the first pharyngeal arch and in the eyes. This expression persists at least until the larval stages. Retinoic acid signaling influences tsh1 expression. Zebrafish tsh1 expression was induced in the anterior neural tube in embryos treated briefly with exogenous retinoic acid. Furthermore, tsh1 expression was down-regulated in the spinal cord in the zebrafish neckless mutant in which RA signaling is disrupted due to a missense mutation in the gene encoding retinaldehyde dehydrogenase type 2.
我们报告了tsh1的表达模式,tsh1是果蝇同源异型基因teashirt的斑马鱼同源物。tsh1的表达最早在受精后10小时(hpf)的2体节期在脊髓前端被检测到。表达向脊髓后端扩展,到prim-5期(24 hpf)时,在整个脊髓中都能检测到tsh1转录本。在14至25体节期(16至24 hpf)之间,脊髓表达在菱脑节7的吻侧边缘显示出清晰的前边界。在prim-25期(36 hpf)左右,虽然tsh1的脊髓表达减少,但在胸鳍芽和背侧前脑中检测到新的表达。到长胸鳍期(48 hpf)时,脊髓表达无法检测到,但在菱脑、端脑、视顶盖、中脑-后脑边界、第一咽弓和眼睛中观察到强烈表达。这种表达至少持续到幼虫阶段。视黄酸信号影响tsh1的表达。用外源性视黄酸短暂处理的胚胎中,tsh1在神经管前部被诱导表达。此外,在斑马鱼无颈突变体中,tsh1在脊髓中的表达下调,在该突变体中,由于编码视网膜醛脱氢酶2的基因中的错义突变,视黄酸信号被破坏。