VillinCre-Blimpflox mice postpartum day 7

In many mammalian species, the intestinal epithelium is immature at birth. During the suckling to weaning transition, the intestine matures. This developmental transition is the result of a genetic program that is intrinsic to the gut and independent of luminal content, but its regulators have not been identified. We investigated the function of the transcriptional repressor Blimp-1 using mice with intestine-specific ablation of Blimp-1. Deletion of Blimp-1 results in growth retardation and excess neonatal mortality. Mutant mice lack all typical epithelial features of the suckling period and are born with features of adult-like intestine. To assess the function of the gene Prdm1 (Blimp) on postnatal day 7 intestinal epithelium, VillinCre-Blimpflox and control (VillinCre-Blimpwt or Cre-Blimpflox) mice were generated. Mice were sacrificed at day 7 postnatal, and pieces of whole mid-intestine were taken for analysis.在诸多哺乳动物物种中，肠上皮（intestinal epithelium）在出生时仍未成熟。在哺乳至断奶的过渡期内，肠道将完成成熟发育。这一发育转变由肠道固有遗传程序驱动，且不依赖肠腔内容物，但其具体调控因子迄今尚未被鉴定。本研究通过构建肠道特异性敲除Blimp-1的小鼠模型，探究了转录抑制因子Blimp-1的功能。敲除Blimp-1会导致小鼠生长迟缓，并提升新生小鼠死亡率。突变型小鼠完全缺失哺乳阶段典型的上皮特征，且出生时即呈现出类似成年个体的肠道表型。为评估基因Prdm1（Blimp-1）在出生后第7天肠上皮中的功能，我们构建了VillinCre-Blimpflox小鼠及其对照组（VillinCre-Blimpwt或Cre-Blimpflox小鼠）。于出生后第7天处死小鼠，摘取完整中段肠组织用于后续分析。