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The Arabidopsis thaliana nucleotide sugar transporter GONST2 is a functional homolog of GONST1.
Glycosylinositolphosphorylceramides (GIPCs) are the predominant lipid in the outer leaflet of the plasma membrane. Characterized GIPC glycosylation mutants have severe or lethal plant phenotypes. However, the function of the glycosylation is unclear. Previously, we characterized Arabidopsis thaliana GONST1 and showed that it was a nucleotide sugar transporter which provides GDP-mannose for GIPC glycosylation. gonst1 has a severe growth phenotype, as well as a constitutive defense response. Here, we characterize a mutant in GONST1's closest homolog, GONST2. The gonst2-1 allele has a minor change to GIPC headgroup glycosylation. Like other reported GIPC glycosylation mutants, gonst1-1gonst2-1 has reduced cellulose, a cell wall polymer that is synthesized at the plasma membrane. The gonst2-1 allele has increased resistance to a biotrophic pathogen Golovinomyces orontii but not the necrotrophic pathogen Botrytis cinerea. Expression of GONST2 under the GONST1 promoter can rescue the gonst1 phenotype, indicating that GONST2 has a similar function to GONST1 in providing GDP-D-Man for GIPC mannosylation
Adenovirus Type 7 Peptide Diversity during Outbreak, Korea, 1995–2000
To understand the molecular basis of observed regional shifts in the genome types of adenovirus type 7 (Ad7) isolated in Korea during nationwide outbreaks from 1995 to 2000, the genetic variabilities of Ad7d and Ad7l were studied by sequence analysis of hexon, fiber, E3, and E4 open reading frame (ORF) 6/7 peptides. One amino acid change in the receptor-binding domain of fiber and 6 amino acid variations in E4 ORF 6/7 were identified between 2 genome types, while no variations were found in hexon and E3. Phylogenetic trees based on hexon, fiber, and E4 suggested that the Ad7 epidemic was probably caused by the introduction of the Japanese Ad7d strains. Our data also provide evidence that the rapid divergence of Ad7d to a novel genome type Ad7l could have been due to viral strategies involving multiple sequence changes in E4. This result suggests fiber and E4 ORF 6/7 peptides participate in the evolution of Ad7
CNVs in Three Psychiatric Disorders
BACKGROUND: We aimed to determine the similarities and differences in the roles of genic and regulatory copy number variations (CNVs) in bipolar disorder (BD), schizophrenia (SCZ), and autism spectrum disorder (ASD).
METHODS: Based on high-resolution CNV data from 8708 Japanese samples, we performed to our knowledge the largest cross-disorder analysis of genic and regulatory CNVs in BD, SCZ, and ASD.
RESULTS: In genic CNVs, we found an increased burden of smaller (500 kb) exonic CNVs in SCZ/ASD. Pathogenic CNVs linked to neurodevelopmental disorders were significantly associated with the risk for each disorder, but BD and SCZ/ASD differed in terms of the effect size (smaller in BD) and subtype distribution of CNVs linked to neurodevelopmental disorders. We identified 3 synaptic genes (DLG2, PCDH15, and ASTN2) as risk factors for BD. Whereas gene set analysis showed that BD-associated pathways were restricted to chromatin biology, SCZ and ASD involved more extensive and similar pathways. Nevertheless, a correlation analysis of gene set results indicated weak but significant pathway similarities between BD and SCZ or ASD (r = 0.25–0.31). In SCZ and ASD, but not BD, CNVs were significantly enriched in enhancers and promoters in brain tissue.
CONCLUSIONS: BD and SCZ/ASD differ in terms of CNV burden, characteristics of CNVs linked to neurodevelopmental disorders, and regulatory CNVs. On the other hand, they have shared molecular mechanisms, including chromatin biology. The BD risk genes identified here could provide insight into the pathogenesis of BD
マウスアデノウイルスカンセンニタイスルサイボウセイメンエキニカンスルケンキュウ
京都大学0048新制・課程博士医学博士甲第2120号医博第510号新制||医||248(附属図書館)5630UT51-53-M100京都大学大学院医学研究科病理系専攻(主査)教授 花岡 正男, 教授 浜島 義博, 教授 植竹 久雄学位規則第5条第1項該当Kyoto UniversityDA
Characterization of lactate dehydrogenase-elevating virus ORF6 protein expressed by recombinant baculoviruses
Lactate dehydrogenase-elevating virus (LDV) has a strict species-specificity and can replicate only in a subset of mouse primary macrophages in vitro. Because it is difficult to grow and purify sufficient quantities of LDV virions from the primary macrophages, it has been difficult to further characterize LDV envelope proteins. A few expression systems have been reported for structural analysis of the nonglycosylated envelope protein M/VP-2, however, very few studies of the antigenicity of M/VP-2 have been reported. We cloned and expressed the ORF6 gene, which encodes the M/VP-2, as a fusion protein with a polyhistidine metal-binding tag (6 x His-tag) in Autographa californica nuclear polyhedrosis virus (baculovirus) under the control of the polyhedrin promoter. In Western blotting analysis, the expressed protein was similar in size to the native M/VP-2 plus 6 x His-tag. The usefulness of the baculovirus-expressed LDV ORF6 protein for analysis of the immunogenicity of LDV M/VP-2 was discussed