Gurling Mark, Garriga Gian
Molecular and Cell Biology; University of California ; Berkeley, CA USA ; Present address: Department of Biochemistry; University of Utah ; Salt Lake City, UT USA.
Molecular and Cell Biology; University of California ; Berkeley, CA USA.
Worm. 2015 Feb 3;4(1):e979697. doi: 10.4161/21624054.2014.979697. eCollection 2015 Jan-Mar.
The C. elegans Q lineage provides a unique context for studying how cells divide asymmetrically to generate cells fated to die. The Q cell divides to form the Q.a and Q.p neuroblasts, each of which divides to produce neurons and a cell that dies by apoptosis; however, these neuroblasts employ different mechanisms to divide asymmetrically.(1) We discovered 2 distinct roles for TOE-2, a protein previously shown to be a target of the C. elegans ERK ortholog MPK-1, in promoting apoptosis in each of these neuroblast divisions. In this commentary, we discuss possible molecular mechanisms by which TOE-2 promotes apoptosis. Specifically, we will discuss potential roles for TOE-2 interacting proteins, a possible nuclear function for TOE-2, and a potential link to the Wnt pathway.
秀丽隐杆线虫的Q细胞谱系为研究细胞如何不对称分裂以产生注定死亡的细胞提供了一个独特的背景。Q细胞分裂形成Q.a和Q.p神经母细胞，每个神经母细胞都会分裂产生神经元和一个通过凋亡死亡的细胞；然而，这些神经母细胞采用不同的机制进行不对称分裂。(1)我们发现了TOE-2的两种不同作用，TOE-2是一种先前被证明是秀丽隐杆线虫ERK直系同源物MPK-1的靶标的蛋白质，在促进这些神经母细胞每次分裂中的凋亡过程中发挥作用。在这篇评论中，我们讨论了TOE-2促进凋亡的可能分子机制。具体来说，我们将讨论TOE-2相互作用蛋白的潜在作用、TOE-2可能的核功能以及与Wnt信号通路的潜在联系。
