Zhao Xiaojun, Sawa Hitoshi, Herman Michael A
Program in Molecular, Cellular and Developmental Biology, Division of Biology, Kansas State University, Manhattan, KS 66506, USA.
Dev Biol. 2003 Apr 15;256(2):276-89. doi: 10.1016/s0012-1606(02)00128-8.
Mutations in tcl-2 cause defects in the specification of the fates of the descendants of the TL and TR blast cells, whose polarity is regulated by lin-44/Wnt and lin-17/frizzled, during Caenorhabditis elegans development. In wild-type animals, POP-1/TCF/LEF, is asymmetrically distributed to the T cell daughters, resulting in a higher level of POP-1 in the nucleus of the anterior daughter. The POP-1 asymmetric distribution is controlled by lin-44 and lin-17. However, in tcl-2 mutants, POP-1 is equally distributed to T cell daughters as is observed in lin-17 mutants, indicating that, like lin-17, tcl-2 functions upstream of pop-1. In addition, tcl-2 mutations cause defects in the development of the gonad and the specification of fate of the posterior daughter of the P12 cell, both of which are controlled by the Wnt pathway. Double mutant analyses indicate that tcl-2 can act synergistically with the Wnt pathway to control gonad development as well as P12 descendant cell fate specification. tcl-2 encodes a novel protein. A functional tcl-2::gfp construct was weakly expressed in the nuclei of the T cell and its descendants. Our results suggest that tcl-2 functions with Wnt pathways to control T cell fate specification, gonad development, and P12 cell fate specification.
在秀丽隐杆线虫发育过程中，tcl-2基因的突变会导致TL和TR原始细胞后代细胞命运特化出现缺陷，这些细胞的极性由lin-44/Wnt和lin-17/卷曲蛋白调控。在野生型动物中，POP-1/TCF/LEF不对称地分布于T细胞子代细胞中，导致前侧子代细胞核中POP-1水平较高。POP-1的不对称分布受lin-44和lin-17控制。然而，在tcl-2突变体中，POP-1像在lin-17突变体中那样均匀地分布于T细胞子代细胞中，这表明tcl-2与lin-17一样，在pop-1的上游发挥作用。此外，tcl-2突变会导致性腺发育缺陷以及P12细胞后侧子代细胞命运特化异常，这两者均受Wnt信号通路控制。双突变分析表明，tcl-2能与Wnt信号通路协同作用，控制性腺发育以及P12后代细胞命运特化。tcl-2编码一种新型蛋白质。一个功能性的tcl-2::gfp构建体在T细胞及其子代细胞的细胞核中弱表达。我们的结果表明，tcl-2与Wnt信号通路共同作用，控制T细胞命运特化、性腺发育以及P12细胞命运特化。
