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Genetic Interactions Reveal that Speci c Defects of Chloroplast Translation are Associated with the Suppression of var2-Mediated Leaf Variegation 被引量:3
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作者 Xiayan Liu Mengdi Zheng +4 位作者 Rui Wang Ruijuan Wang Lijun An Steve R.Rodermel Fei Yu 《Journal of Integrative Plant Biology》 SCIE CAS CSCD 2013年第10期979-993,共15页
Arabidopsis thaliana L. yellow variegated (var2) mutant is defective in a chloroplast FtsH family metalloprotease, AtFtsH2/VAR2, and displays an intriguing green and white leaf variegation. This unique var2-mediated... Arabidopsis thaliana L. yellow variegated (var2) mutant is defective in a chloroplast FtsH family metalloprotease, AtFtsH2/VAR2, and displays an intriguing green and white leaf variegation. This unique var2-mediated leaf variegation offers a simple yet powerful tool for dissecting the genetic regulation of chloroplast development. Here, we report the isolation and characterization of a new var2 suppressor gene, SUPPRESSOR OF VARIEGA TION8 (SVR8), which encodes a putative chloroplast ribosomal large subunit protein, L24. Mutations in SVR8 suppress var2 leaf variegation at ambient temperature and partially suppress the cold-induced chlorosis phenotype of var2. Loss of SVR8 causes unique chloroplast rRNA processing defects, particularly the 23S-4.5S dicistronic precursor. The recovery of the major abnormal processing site in svr823S-4.5S precursor indicate that it does not lie in the same position where SVR8/L24 binds on the ribosome. Surprisingly, we found that the loss of a chloroplast ribosomal small subunit protein, $21, results in aberrant chloroplast rRNA processing but not suppression of var2 variegation. These findings suggest that the disruption of specific aspects of chloroplast translation, rather than a general impairment in chloroplast translation, suppress var2variegation and the existence of complex genetic interactions in chloroplast development. 展开更多
关键词 Chloroplast ribosomal protein L24 chloroplast rRNA processing genetic suppressor leaf variegation var2.
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Identification of mutation in a candidate gene for hereditary multiple exostoses type Ⅱ
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作者 徐磊 邓汉湘 +5 位作者 夏家辉 李贺君 周江南 王大平 潘乾 龙志高 《Chinese Medical Journal》 SCIE CAS CSCD 1999年第1期73-76,共4页
Objectives To identify possible mutations in our previously cloned candidate gene for hereditary multiple exostoses type Ⅱ (EXT2) in affected members of EXT families so as to confirm that it is the disease causing ... Objectives To identify possible mutations in our previously cloned candidate gene for hereditary multiple exostoses type Ⅱ (EXT2) in affected members of EXT families so as to confirm that it is the disease causing gene. Methods The mutation was detected first by single strand conformational polymorphism(SSCP) of all coding exons of the candidate gene and then by sequencing analysis. Results After analyzing 37 patients from 20 Chinese EXT families by SSCP and DNA sequencing analysis, one 2 bp insertion mutation was identified in this candidate gene in affected members of an EXT family. This mutation resulted in the frameshift and generated a truncated gene product consisting of 105 amino acids. Conclusions The identification of the mutation in the candidate gene indicates that this novel gene is responsible for EXT2 (one of the disease causing gene of EXT). 展开更多
关键词 hereditary multiple exostoses positional cloning MUTATION tumor suppressor gene National Laboratory of Medical genetics Hunan Medical University Changsha 410078 China (Xu L Deng HX Xia JH Pan Q and Long ZG) Department of Osteology
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