Bowerman B, Ingram M K, Hunter C P
Institute of Molecular Biology, University of Oregon, Eugene 97403, USA.
Development. 1997 Oct;124(19):3815-26. doi: 10.1242/dev.124.19.3815.
After fertilization in C. elegans, activities encoded by the maternally expressed par genes appear to establish cellular and embryonic polarity. Loss-of-function mutations in the par genes disrupt anterior-posterior (a-p) asymmetries in early embryos and result in highly abnormal patterns of cell fate. Little is known about how the early asymmetry defects are related to the cell fate patterning defects in par mutant embryos, or about how the par gene products affect the localization and activities of developmental regulators known to specify the cell fate patterns made by individual blastomeres. Examples of such regulators of blastomere identity include the maternal proteins MEX-3 and GLP-1, expressed at high levels anteriorly, and SKN-1 and PAL-1, expressed at high levels posteriorly in early embryos. To better define par gene functions, we examined the expression patterns of MEX-3, PAL-1 and SKN-1, and we analyzed mex-3, pal-1, skn-1 and glp-1 activities in par mutant embryos. We have found that mutational inactivation of each par gene results in a unique phenotype, but in no case do we observe a complete loss of a-p asymmetry. We conclude that no one par gene is required for all a-p asymmetry and we suggest that, in some cases, the par genes act independently of each other to control cell fate patterning and polarity. Finally, we discuss the implications of our findings for understanding how the initial establishment of polarity in the zygote by the par gene products leads to the proper localization of more specifically acting regulators of blastomere identity.
在秀丽隐杆线虫受精后，母源表达的par基因所编码的活性似乎能建立细胞和胚胎极性。par基因的功能丧失突变会破坏早期胚胎的前后（a-p）不对称性，并导致细胞命运模式高度异常。关于早期不对称缺陷如何与par突变胚胎中的细胞命运模式缺陷相关，或者par基因产物如何影响已知能指定单个卵裂球所形成的细胞命运模式的发育调节因子的定位和活性，我们知之甚少。此类卵裂球身份调节因子的例子包括母源蛋白MEX-3和GLP-1，它们在早期胚胎的前部高水平表达，以及SKN-1和PAL-1，它们在早期胚胎的后部高水平表达。为了更好地界定par基因的功能，我们检测了MEX-3、PAL-1和SKN-1的表达模式，并分析了par突变胚胎中的mex-3、pal-1、skn-1和glp-1活性。我们发现每个par基因的突变失活都会导致独特的表型，但在任何情况下我们都未观察到a-p不对称性的完全丧失。我们得出结论，并非所有a-p不对称性都需要单个par基因，并且我们认为，在某些情况下，par基因彼此独立发挥作用以控制细胞命运模式和极性。最后，我们讨论了我们的发现对于理解par基因产物如何在合子中最初建立极性从而导致更特异性作用的卵裂球身份调节因子的正确定位的意义。
