在同时缺乏JNK1和JNK2的情况下，神经管形态发生缺陷且细胞凋亡改变。

Defective neural tube morphogenesis and altered apoptosis in the absence of both JNK1 and JNK2.

作者信息

Sabapathy K, Jochum W, Hochedlinger K, Chang L, Karin M, Wagner E F

机构信息

Research Institute of Molecular Pathology, Dr. Bohr-Gasse 7, A-1030, Vienna, Austria.

出版信息

Mech Dev. 1999 Dec;89(1-2):115-24. doi: 10.1016/s0925-4773(99)00213-0.

DOI:10.1016/s0925-4773(99)00213-0

PMID:10559486

Abstract

Mice lacking both c-Jun-NH(2)-terminal kinases (JNK1 and JNK2) were generated to define their roles in development. Jnk1/jnk2 double mutant fetuses die around embryonic day 11 (E11) and were found to display an open neural tube (exencephaly) at the hindbrain level with reduced apoptosis in the hindbrain neuroepithelium at E9.25. In contrast, a dramatic increase in cell death was observed one day later at E10.5 in both the hindbrain and forebrain regions. Moreover, about 25% of jnk1-/-jnk2+/- fetuses display exencephaly probably due to reduced levels of JNK proteins, whereas jnk1+/-jnk2-/- mice are viable. These results assign both pro- and anti-apoptotic functions for JNK1 and JNK2 in the development of the fetal brain.

摘要

为了确定c-Jun氨基末端激酶（JNK1和JNK2）在发育中的作用，构建了同时缺乏这两种激酶的小鼠。Jnk1/jnk2双突变体胎儿在胚胎第11天（E11）左右死亡，并且发现在E9.25时后脑海马区出现开放性神经管（无脑畸形），后脑海马神经上皮细胞凋亡减少。相比之下，在一天后的E10.5时，在后脑和前脑区域均观察到细胞死亡显著增加。此外，约25%的jnk1-/-jnk2+/-胎儿可能由于JNK蛋白水平降低而出现无脑畸形，而jnk1+/-jnk2-/-小鼠是可存活的。这些结果表明JNK1和JNK2在胎儿大脑发育中具有促凋亡和抗凋亡功能。