A stem cell-derived gene (Sddr) negatively regulates differentiation of embryonic stem cells

金沢大学医薬保健研究域医学系Embryonic stem (ES) cells, derived from the inner cell mass of blastocysts, are pluripotent and continue to self-renew. To better understand the molecular mechanisms under-lying self-renewal, we have been searching for a gene(s) which is specifically expressed in self-renewing ES cells. Here we report the isolation and characterization of a novel gene, Sddr (stem cell-derived differentiation regulator). Sddr was highly expressed in undifferentiated ES cells, and its expression was downregulated upon differentiation. In addition to ES cells, Sddr expression was observed strongly in ovary, and weakly in lung. Immunostaining and cellular fractionation analyses suggested that Sddr is a cytoplasmic protein associated with the cytoskeleton. Sddr-null ES cells showed no remarkable abnormalities in their undifferentiated state. In contrast, in differentiating Sddr-null cells, induction of several differentiation-associated markers was enhanced, and downregulation of self-renewal marker genes was accelerated, as compared with wild-type cells. These results suggest that although it is dispensable for ES cell self-renewal, Sddr is a negative regulator of ES cell differentiation. © 2009 UBC Press

Genetic and antigenic characterisation of influenza A(H3N2) viruses isolated in Yokohama during the 2016/17 and 2017/18 influenza seasons.

BACKGROUND: Influenza A(H3N2) virus rapidly evolves to evade human immune responses, resulting in changes in the antigenicity of haemagglutinin (HA). Therefore, continuous genetic and antigenic analyses of A(H3N2) virus are necessary to detect antigenic mutants as quickly as possible. AIM: We attempted to phylogenetically and antigenically capture the epidemic trend of A(H3N2) virus infection in Yokohama, Japan during the 2016/17 and 2017/18 influenza seasons. METHODS: We determined the HA sequences of A(H3N2) viruses detected in Yokohama, Japan during the 2016/17 and 2017/18 influenza seasons to identify amino acid substitutions and the loss or gain of potential N-glycosylation sites in HA, both of which potentially affect the antigenicity of HA. We also examined the antigenicity of isolates using ferret antisera obtained from experimentally infected ferrets. RESULTS: Influenza A(H3N2) viruses belonging to six clades (clades 3C.2A1, 3C.2A1a, 3C.2A1b, 3C.2A2, 3C.2A3 and 3C.2A4) were detected during the 2016/17 influenza season, whereas viruses belonging to two clades (clades 3C.2A1b and 3C.2A2) dominated during the 2017/18 influenza season. The isolates in clades 3C.2A1a and 3C.2A3 lost one N-linked glycosylation site in HA relative to other clades. Antigenic analysis revealed antigenic differences among clades, especially clade 3C.2A2 and 3C.2A4 viruses, which showed distinct antigenic differences from each other and from other clades in the antigenic map. CONCLUSION: Multiple clades, some of which differed antigenically from others, co-circulated in Yokohama, Japan during the 2016/17 and 2017/18 influenza seasons

Mapping a QTL conferring resistance to Fusarium head blight on chromosome 1B in winter wheat (<i>Triticum aestivum</i> L.)

Fusarium head blight (FHB) is one of the most devastating diseases of wheat (Triticum aestivum L.), and the development of cultivars with FHB resistance is the most effective way to control the disease. Yumechikara is a Japanese hard red winter wheat cultivar that shows moderate resistance to FHB with superior bread-making quality. To identify quantitative trait loci (QTLs) for FHB resistance in Yumechikara, we evaluated doubled haploid lines derived from a cross between Yumechikara and a moderate susceptible cultivar, Kitahonami, for FHB resistance in a 5-year field trial, and we analyzed polymorphic molecular markers between the parents. Our analysis of these markers identified two FHB-resistance QTLs, one from Yumechikara and one from Kitahonami. The QTL from Yumechikara, which explained 36.4% of the phenotypic variation, was mapped on the distal region of chromosome 1BS, which is closely linked to the low-molecular-weight glutenin subunit gene Glu-B3 and the glume color gene Rg-B1. The other QTL (from Kitahonami) was mapped on chromosome 3BS, which explained 11.2% of the phenotypic variation. The close linkage between the FHB-resistance QTL on 1BS, Glu-B3 and Rg-B1 brings an additional value of simultaneous screening for both quality and FHB resistance using the glume color