在果蝇神经发生过程中，miti-mere基因和pdm1基因在RP2/sib细胞系的特化过程中相互协作。
The miti-mere and pdm1 genes collaborate during specification of the RP2/sib lineage in Drosophila neurogenesis.
作者信息
Bhat K M, Poole S J, Schedl P
机构信息
Department of Molecular Biology, Princeton University, New Jersey 08544, USA.
出版信息
Mol Cell Biol. 1995 Aug;15(8):4052-63. doi: 10.1128/MCB.15.8.4052.
Abstract
We have investigated (i) the role of pdm1, a Drosophila POU gene, during the elaboration of the GMC-1-->RP2/sib lineage and (ii) the functional relationship between pdm1 and the closely linked second POU gene, miti-mere, in this lineage. We show that deletion of pdm1 causes a partially penetrant GMC-1 defect, while deletion of both miti and pdm1 results in a fully penetrant defect. This GMC-1 defect in miti- and pdm1- embryos can be rescued by the pdm1 or miti transgene. Rescue is observed only when these genes are expressed at the time of GMC-1 formation. Overexpression of pdm1 or miti well after GMC-1 is formed results in the duplication of RP2 and/or sib cells. Our results indicate that both genes are required for the normal development of this lineage and that the two collaborate during the specification of GMC-1 identity.
摘要
我们研究了（i）果蝇POU基因pdm1在GMC-1向RP2/sib细胞系分化过程中的作用，以及（ii）在该细胞系中pdm1与紧密连锁的第二个POU基因miti-mere之间的功能关系。我们发现，pdm1的缺失会导致部分GMC-1缺陷，而miti和pdm1同时缺失则会导致完全显性的缺陷。miti和pdm1双缺失胚胎中的这种GMC-1缺陷可被pdm1或miti转基因挽救。只有当这些基因在GMC-1形成时表达时，才能观察到挽救效果。在GMC-1形成后过表达pdm1或miti会导致RP2和/或sib细胞的复制。我们的结果表明，这两个基因对于该细胞系的正常发育都是必需的，并且在GMC-1身份的特化过程中两者相互协作。
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