Levanon Ditsa, Groner Yoram
Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel.
Blood Cells Mol Dis. 2009 Jul-Aug;43(1):1-5. doi: 10.1016/j.bcmd.2009.01.009. Epub 2009 Feb 23.
Runx3 is one of the three mammalian Runt domain transcription factors comprising the deeply conserved RUNX gene family. While the three proteins recognize the same DNA-motif, the functional overlaps are minor; each Runx has a distinct subset of biological functions. This lack of functional redundancy is the consequence of a tightly regulated spatio/temporal expression of the genes by transcriptional and post-transcriptional control mechanisms. Over the years several groups created Runx3-deficient mouse models. Analysis of these mice revealed various phenotypic features that result from loss of cell autonomous function of Runx3. Here we summarize the phenotypic similarities and dissimilarities between two of the Runx3-deficient mouse strains, discuss the basis of the discrepancies and highlight the crux of the dispute.
Runx3是构成高度保守的RUNX基因家族的三种哺乳动物Runt结构域转录因子之一。虽然这三种蛋白质识别相同的DNA基序,但功能重叠较小;每种Runx都有独特的生物学功能子集。这种缺乏功能冗余是通过转录和转录后控制机制对基因进行严格调控的时空表达的结果。多年来,几个研究小组创建了Runx3缺陷型小鼠模型。对这些小鼠的分析揭示了由于Runx3细胞自主功能丧失而导致的各种表型特征。在这里,我们总结了两种Runx3缺陷型小鼠品系之间的表型异同,讨论了差异的基础,并突出了争议的关键。