Blimp1 regulates the transition of neonatal to adult intestinal epithelium

Abstract

In many mammalian species, the intestinal epithelium undergoes major changes that allow a dietary transition from mother's milk to the adult diet at the end of the suckling period. These complex developmental changes are the result of a genetic programme intrinsic to the gut tube, but its regulators have not been identified. Here we show that transcriptional repressor B lymphocyte-induced maturation protein 1 (Blimp1) is highly expressed in the developing and postnatal intestinal epithelium until the suckling to weaning transition. Intestine-specific deletion of Blimp1 results in growth retardation and excessive neonatal mortality. Mutant mice lack all of the typical epithelial features of the suckling period and are born with features of an adult-like intestine. We conclude that the suckling to weaning transition is regulated by a single transcriptional repressor that delays epithelial maturation.

Thyroid Hormone Activates Protein Arginine Methyltransferase 1 Expression by Directly Inducing c-Myc Transcription during Xenopus Intestinal Stem Cell Development

“…Thus, although neonatal mouse intestine is structurally developed, with the proper crypt-villus organization similar to that in the adult mouse, the embryonic/neonatal mouse intestinal stem cells are molecularly distinct from those in the adult mouse intestine (5,6,46). This conclusion is also supported by recent studies on the transcription repressor, B lymphocyte-induced maturation protein 1 (Blimp1) (53,54). Blimp1 is strongly expressed throughout the intestinal epithelium before birth.…”

“…The formation of the adult intestine is highly conserved among vertebrates and takes place through the formation of adult epithelial stem cells during postembryonic development when T3 levels are high (5,6,46,53,54). In anurans, this corresponds to the metamorphic period.…”

Identification and expression profiles of prdm1 in medaka Oryzias latipes

“…However, no observation of prdm1a was in the primordial germ cells (PGCs) of medaka. These results hinted that medaka Prdm1a possibly has similar function as its homologues of zebrafish and mouse in development of muscle [38,46], neural crest [41,46], branchial arches [46], fin [43,44,46], eye [29,55], intestine [30,31], heart [28] and bone [56]. In mouse, Prdm1 plays its role itself and/or through its partner factors, Prmt5 and/or Groucho proteins [9,25].…”

“…Except of functions in immune-related cells, Prdm1 plays key roles in the development of a wide variety of tissues in mice [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36]. In mice, Prdm1 is expressed in endoderm, mesoderm and ectoderm-derived tissues during embryonic development [37].…”

“…In mice, Prdm1 is expressed in endoderm, mesoderm and ectoderm-derived tissues during embryonic development [37]. Prdm1 governs germ cell specification [23][24][25] and regulates development of the sebaceous gland [26], skin epidermis [27], the posterior forelimb, caudal pharyngeal arches, sensory vibrissae, heart [28], photoreceptor [29], and intestine [30,31]. Prdm1 also is a tumor suppressor in blood cells [32][33][34][35] by regulating P53 expression [36].…”