Ch'ng QueeLim, Williams Lisa, Lie Yung S, Sym Mary, Whangbo Jennifer, Kenyon Cynthia
Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94143-0448, USA.
Genetics. 2003 Aug;164(4):1355-67. doi: 10.1093/genetics/164.4.1355.
In C. elegans, cells of the QL and QR neuroblast lineages migrate with left-right asymmetry; QL and its descendants migrate posteriorly whereas QR and its descendants migrate anteriorly. One key step in generating this asymmetry is the expression of the Hox gene mab-5 in the QL descendants but not in the QR descendants. This asymmetry appears to be coupled to the asymmetric polarizations and movements of QL and QR as they migrate and relies on an asymmetric response to an EGL-20/Wnt signal. To identify genes involved in these complex layers of regulation and to isolate targets of mab-5 that direct posterior migrations, we screened visually for mutants with cell migration defects in the QL and QR lineages. Here, we describe a set of new mutants (qid-5, qid-6, qid-7, and qid-8) that primarily disrupt the migrations of the QL descendants. Most of these mutants were defective in mab-5 expression in the QL lineage and might identify genes that interact directly or indirectly with the EGL-20/Wnt signaling pathway.
在秀丽隐杆线虫中，QL和QR神经母细胞谱系的细胞以左右不对称的方式迁移；QL及其后代向后迁移，而QR及其后代向前迁移。产生这种不对称性的一个关键步骤是Hox基因mab-5在QL后代中表达，而不在QR后代中表达。这种不对称性似乎与QL和QR迁移时的不对称极化和运动相关，并依赖于对EGL-20/Wnt信号的不对称反应。为了鉴定参与这些复杂调控层次的基因，并分离出指导向后迁移的mab-5靶标，我们通过视觉筛选了QL和QR谱系中具有细胞迁移缺陷的突变体。在这里，我们描述了一组新的突变体（qid-5、qid-6、qid-7和qid-8），它们主要破坏QL后代的迁移。这些突变体中的大多数在QL谱系中mab-5的表达存在缺陷，可能鉴定出直接或间接与EGL-20/Wnt信号通路相互作用的基因。
