Defective cranial skeletal development, larval lethality and haploinsufficiency in Myod mutant zebrafish.
Defective cranial skeletal development, larval lethality and haploinsufficiency in Myod mutant zebrafish.
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DOI：
10.1016/j.ydbio.2011.07.015
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发表时间：
2011-10-01
影响因子：
2.7
通讯作者：
Hughes SM
中科院分区：
文献类型：
--
作者：
Hinits Y;Williams VC;Sweetman D;Donn TM;Ma TP;Moens CB;Hughes SM
肌源性调节因子家族（MRFs）是哺乳动物骨骼肌发生所必需的转录因子。在这里，我们表明，在斑马鱼myod基因的突变延迟和减少早期体节和胸鳍肌发生，减少miR-206的表达，并导致体节大小持续减少，直到至少独立的喂养阶段。编码第二个MRF的myog突变在早期阶段几乎没有明显的表型，但加剧了由于缺乏Myod引起的体节肌的损失。myod和myf 5的突变会消融所有骨骼肌。myod的单倍不足导致胚胎体节肌肉体积减少。缺乏Myod会导致颅部肌肉组织严重减少，包括推定的兜状肌同源物-胸长肌在内的大部分肌肉消融。这种表型伴随着软骨骨骼的严重畸形和几个颅骨（包括鳃盖骨）的成熟失败。由于myod的表达仅限于生肌细胞，因此数据表明，肌生成对于头部的适当骨骼发生是必不可少的。
Myogenic regulatory factors of the myod family (MRFs) are transcription factors essential for mammalian skeletal myogenesis. Here we show that a mutation in the zebrafish myod gene delays and reduces early somitic and pectoral fin myogenesis, reduces miR-206 expression, and leads to a persistent reduction in somite size until at least the independent feeding stage. A mutation in myog, encoding a second MRF, has little obvious phenotype at early stages, but exacerbates the loss of somitic muscle caused by lack of Myod. Mutation of both myod and myf5 ablates all skeletal muscle. Haploinsufficiency of myod leads to reduced embryonic somite muscle bulk. Lack of Myod causes a severe reduction in cranial musculature, ablating most muscles including the protractor pectoralis, a putative cucullaris homologue. This phenotype is accompanied by a severe dysmorphology of the cartilaginous skeleton and failure of maturation of several cranial bones, including the opercle. As myod expression is restricted to myogenic cells, the data show that myogenesis is essential for proper skeletogenesis in the head.
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影响因子：
--
作者：
Diogo R;Hinits Y;Hughes SM
通讯作者：
Hughes SM
影响因子：
4.6
作者：
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通讯作者：
Hughes, Simon M.
影响因子：
4.6
作者：
Hinits, Yaniv;Hughes, Simon M.
通讯作者：
Hughes, Simon M.
影响因子：
4.6
作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
Kirby, ML