Miyoshi Tomoya, Maruhashi Mitsuji, Van De Putte Tom, Kondoh Hisato, Huylebroeck Danny, Higashi Yujiro
Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Dev Dyn. 2006 Jul;235(7):1941-52. doi: 10.1002/dvdy.20799.
In mouse embryos, the Zfhx1 transcription factor genes, Sip1 and deltaEF1, are expressed in complementary domains in many tissues. Their possible synergism in embryogenesis was investigated by comparing the phenotype of Sip1-/-;deltaEF1-/- double homozygotes with single homozygous embryos. Unexpectedly, in Sip1-/- embryos deltaEF1 was ectopically activated, suggesting a negative regulation of deltaEF1 expression by Sip1. Sip1-/-;deltaEF1-/- embryos were similar to Sip1-/- embryos in short somite production and developmental arrest around E8.5, but showed more severe defects in dorsal neural tube morphogenesis accompanied by a larger reduction of Sox2 expression, ascribable to the loss of the ectopic deltaEF1 expression. Sip1+/-;deltaEF1-/- embryos develop various morphological defects after E10 that were absent in deltaEF1-/- embryos even in tissues without significant overlap of Sip1 and deltaEF1 expression, and arrested during mid gestation earlier than deltaEF1-/- embryos. These findings indicate that complex synergistic interactions occur between Zfhx1 transcription factor genes during mouse embryogenesis.
在小鼠胚胎中,Zfhx1转录因子基因Sip1和deltaEF1在许多组织的互补区域表达。通过比较Sip1-/-;deltaEF1-/-双纯合子与单纯合子胚胎的表型,研究了它们在胚胎发生过程中可能的协同作用。出乎意料的是,在Sip1-/-胚胎中,deltaEF1被异位激活,这表明Sip1对deltaEF1的表达具有负调控作用。Sip1-/-;deltaEF1-/-胚胎在短体节产生和E8.5左右的发育停滞方面与Sip1-/-胚胎相似,但在背神经管形态发生方面表现出更严重的缺陷,同时Sox2表达的降低幅度更大,这可归因于异位deltaEF1表达的缺失。Sip1+/-;deltaEF1-/-胚胎在E10后出现各种形态缺陷,这些缺陷在deltaEF1-/-胚胎中不存在,即使在Sip1和deltaEF1表达没有明显重叠的组织中也是如此,并且比deltaEF1-/-胚胎更早地在妊娠中期停滞发育。这些发现表明,在小鼠胚胎发生过程中,Zfhx1转录因子基因之间发生了复杂的协同相互作用。