Huang Yongzhao, Roelink Henk, McKnight G Stanley
Department of Pharmacology, University of Washington School of Medicine, Seattle, Washington 98195, USA.
J Biol Chem. 2002 May 31;277(22):19889-96. doi: 10.1074/jbc.M111412200. Epub 2002 Mar 8.
We have studied the function of protein kinase A (PKA) during embryonic development using a PKA-deficient mouse that retains only one functional catalytic subunit allele, either Calpha or Cbeta, of PKA. The reduced PKA activity results in neural tube defects that are specifically localized posterior to the forelimb buds and lead to spina bifida. The affected neural tube has closed appropriately but exhibits an enlarged lumen and abnormal neuroepithelium. Decreased PKA activity causes dorsal expansion of Sonic hedgehog signal response in the thoracic to sacral regions correlating with the regions of morphological abnormalities. Other regions of the neural tube appear normal. The regional sensitivity to changes in PKA activity indicates that downstream signaling pathways differ along the anterior-posterior axis and suggests a functional role for PKA activation in neural tube development.
我们利用一种PKA缺陷型小鼠研究了蛋白激酶A(PKA)在胚胎发育过程中的功能,该小鼠仅保留PKA的一个功能性催化亚基等位基因,即Cα或Cβ。PKA活性降低会导致神经管缺陷,这些缺陷特定地位于前肢芽后方,并导致脊柱裂。受影响的神经管已正常闭合,但管腔扩大且神经上皮异常。PKA活性降低导致胸段至骶段区域中 Sonic hedgehog信号反应的背侧扩展,这与形态异常区域相关。神经管的其他区域看起来正常。对PKA活性变化的区域敏感性表明,下游信号通路沿前后轴存在差异,并提示PKA激活在神经管发育中具有功能性作用。