Loss of the Sall3 gene leads to palate deficiency, abnormalities in cranial nerves, and perinatal lethality
Loss of the Sall3 gene leads to palate deficiency, abnormalities in cranial nerves, and perinatal lethality
复制标题
DOI：
10.1128/mcb.24.16.7102-7112.2004
复制
发表时间：
2004-08-01
影响因子：
5.3
通讯作者：
Monaghan, AP
中科院分区：
文献类型：
--
作者：
Parrish, M;Ott, T;Monaghan, AP
Spalt基因家族的成员编码由7到9个C2H2锌指基序表征的转录因子。在小鼠中已鉴定出4个基因- spalt]至Spalt4 （Sall1至Sall4）。Spalt同源基因在胚胎发生早期在神经和中胚层组织中广泛表达。Sall3在小鼠胚胎第7天（E7）开始在神经外胚层和原始条纹中正常表达，随后在大脑、周围神经、脊髓、肢体芽、腭、心脏和耳小泡中表达。我们已经在小鼠体内产生了一种靶向破坏Sall3的方法。纯合子突变动物在出生后第一天死亡，不能进食。这些动物的口腔结构检查显示，从E16.5开始，在上颚和会厌中存在异常。在E10.5胚胎中，观察到通常支配口腔结构的颅神经，特别是舌咽神经（IX）的缺陷。这些研究表明，Sall3对于后脑神经的发育和相邻鳃弓衍生物的形成是必需的。
Members of the Spalt gene family encode putative transcription factors characterized by seven to nine C2H2 zinc finger motifs. Four genes have been identified in mice-Spalt] to Spalt4 (Sall1 to Sall4). Spalt homologues are widely expressed in neural and mesodermal tissues during early embryogenesis. Sall3 is normally expressed in mice from embryonic day 7 (E7) in the neural ectoderm and primitive streak and subsequently in the brain, peripheral nerves, spinal cord, limb buds, palate, heart, and otic vesicles. We have generated a targeted disruption of Sall3 in mice. Homozygous mutant animals die on the first postnatal day and fail to feed. Examination of the oral structures of these animals revealed that abnormalities were present in the palate and epiglottis from E16.5. In E10.5 embryos, deficiencies in cranial nerves that normally innervate oral structures, particularly the glossopharyngeal nerve (IX), were observed. These studies indicate that Sall3 is required for the development of nerves that are derived from the hindbrain and for the formation of adjacent branchial arch derivatives.