Biomedical subjects

Norifumi Tatsumi

Publications and source records attributed to Norifumi Tatsumi.

3 recordsLinked to original sources

PubMed2026

Two Paralogues as They Like It: Conserved and Divergent Evolution of Vertebrate Gcm Genes.

Gcm1 and Gcm2 are paralogous transcription factors in vertebrates that play key roles in the development of pharyngeal-derived epithelia, yet their deployment across vertebrate lineages remains incompletely understood. While Gcm2 shows deeply conserved pharyngeal expression across gnathostomes, Gcm1 has been mainly characterized in mammals, where it exhibits broader expression patterns. How Gcm1 is deployed in non-mammalian vertebrates has remained unexplored. Here, we performed a comparative analysis of Gcm1 expression in cartilaginous fishes, non-teleost actinopterygians, and amphibians. RNA in situ hybridization revealed conserved Gcm1 expression in gill epithelia across these taxa. Parallel analyses showed that Gcm2 is also expressed in gill epithelia, with overlapping but distinct spatial patterns. In addition, Gcm1 showed lineage-specific expression in bichir embryos, including strong expression in external gills and scattered epithelial cells in the yolk-sac membrane. In the external gills, Gcm1-positive cells possess vacuole-like cytoplasmic structures, suggesting a previously unrecognized epithelial cell population. Together, our findings indicate that Gcm1 and Gcm2 share ancestral expression in pharyngeal epithelia but have followed distinct evolutionary trajectories, with Gcm1 exhibiting greater lineage-specific diversification.

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PubMed2006

Id3 is important for proliferation and differentiation of the hepatoblasts during the chick liver development.

The specified hepatic endoderm (hepatoblasts), the bipotential progenitor for hepatocytes and bile duct epithelial cells, proliferates during the primordial stages of liver development. Despite extensive studies, the mechanism that regulates proliferation of bipotential hepatoblasts is not fully understood. Here we show that Id3, a negative regulator of helix-loop-helix transcription factors, is an important regulator of hepatoblast proliferation in the developing chick liver. Id3 was expressed in hepatoblasts at early developmental stages (stages 12-29) but not in hepatocytes at later developmental stages (stage 34 onwards). Depletion of Id3 in hepatoblasts by siRNA results in failure of cell proliferation, but is not associated with either cell death or failure of expression of Hhex and Fibrinogen, the earliest hepatoblast markers. These observations suggest that at early developmental stages, Id3 functions as a positive regulator of hepatoblast proliferation, independent of cell death or maintenance of the non-terminally differentiated state. Interestingly at later developmental stages, the expression pattern of Id3 is complementary to that of Albumin, a marker of mature hepatocytes. Overexpression of Id3 in liver explants delayed the initiation of Albumin expression. Taken together, our observations show that Id3 is not only a positive regulator of hepatoblast proliferation, but also an inhibitor of their differentiation into hepatocytes in the developing chick liver.

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PubMed2005

Analysis of gene expression patterns in the developing chick liver.

The chick embryo has been used widely for studying liver development. However, in the past 30 years, the usage has decreased markedly due to lack of appropriate marker genes for differentiation in the developing chick liver. To use the chick embryo for analyzing the molecular mechanism of liver development, we surveyed marker genes in the developing chick liver by examining the expression pattern of genes that are well-characterized in the developing mammalian liver. By whole-mount in situ hybridization, Fibrinogen-gamma (FIB) expression was first detected at stage 12, specifically in the anterior intestinal portal, and its liver-specific expression persisted in the later stages. Albumin (ALB) expression was first detected at stage 30, when the liver starts maturing. Cytokeratin 19 (CK19) was first detected at stage 37 in the ductal plate of the liver, and its expression continued in the intrahepatic bile ducts derived from the ductal plate. Hex, a transcription factor, is an additional marker of bile duct differentiation. Hence, FIB, ALB, and CK19 expression can be used to trace hepatic induction, maturation, and bile duct differentiation, respectively.

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