|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Four kinds of ENU-induced white spot mice and chromosome locations of the mutant genes显示文摘Phenotype-driven is the name for an ap-proach used to study gene functions through mutagenesis, location and cloning of the mutant gene. In this study, 150 male C57BL/6J(B6) mice were treated with ENU and repro-duced a total offspring of 3860. Of these descendants, 210 exhibited mutation phenotypes by screening, and more than 10 of them are hereditable. Four kinds of mutant mice, named Wbct, W-1Bao, W-2Bao, and W-3Bao, showed dominant hereditary white spot mutation with partial albinism on their belly, distal limbs and tail terminal. To map these mutant genes, 39 microsatellites, equally distributed on the mouse genome and with difference between B6 and DBA/2J (D2), were selected to scan the genome after discrimination of the white spots in the F2 mice [(B6×D2)×D2]. It is found that, the log odds score (LODS) between W-1Bao and D5Mit168 is 0.56, and the LODS of W-1Bao and D5Mit352 is 4.47. With the gradual application of microsatellites D5Mit290, D5Mit312, D5Mit308 and D5Mit356 that are close to the mutant gene, and the number of F2 mice going up to 537, the mutant W-1Bao is located between D5Mit356 and D5Mit308 on chro-mosome 5, about 42.19 cM from the centromere. In the same way, W-2Bao and W-3Bao are mapped nearby W-1Bao, and Wbct is located on chromosome 1, about 41.6 cM from the centro-mere. After searching for the mouse genome database (MGD) and performing a one-by-one study of all genes located on chromosome subregion, it is believed that the kit gene is an excellent candidate for the white spot mutations of W-1Bao, W-2Bao and W-3Bao. | WU Baojin1,2, MAO Huihua1, SHAO Yixiang1, XUE Zhengfeng1 & LI Houda1 1. Comparative Medicine Center of Yangzhou University, Yangzhou 225009, China 2. Medical College of Yangzhou University, Yangzhou 225001, China Correspondence should be addressed to Li Houda (e-mail: houdali @yahoo.com.cn) | 2003 | Chinese Science Bulletin2003，48，24： | 11 |
| 2 | Rice FLOURY ENDOSPERM 18 encodes a pentatricopeptide repeat protein required for 5′ processing of mitochondrial nad5 messenger RNA and endosperm development显示文摘Pentatricopeptide repeat(PPR) proteins, composing one of the largest protein families in plants,are involved in RNA binding and regulation of organelle RNA metabolism at the posttranscriptional level. Although several PPR proteins have been implicated in endosperm development in rice(Oryza sativa), the molecular functions of many PPRs remain obscure. Here, we identified a rice endosperm mutant named floury endosperm 18(flo18) with pleiotropic defects in both reproductive and vegetative development.Map-based cloning and complementation tests showed that FLO18 encodes a mitochondriontargeted P-type PPR protein with 15 PPR motifs.Mitochondrial function was disrupted in the flo18 mutant, as evidenced by decreased assembly of Complex I in the mitochondrial electron transport chain and altered mitochondrial morphology. Loss of FLO18 function resulted in defective 5′-end processing of mitochondrial nad5 transcripts encoding subunit 5 of nicotinamide adenine dinucleotide hydrogenase. These results suggested that FLO18 is involved in 5′-end processing of nad5 messenger RNA and plays an important role in mitochondrial function and endosperm development. | Mingzhou Yu Mingming Wu Yulong Ren Yihua Wang Jingfang Li Cailin Lei Yinglun Sun Xiuhao Bao Hongming Wu Hang Yang Tian Pan Yongfei Wang Ruonan Jing Mengyuan Yan Houda Zhang Lei Zhao Zhichao Zhao Xin Zhang Xiuping Guo Zhijun Cheng Bing Yang Ling Jiang Jianmin Wan | 2021 | Journal of Integrative Plant Biology2021，63，5： | 2 |
| 3 | Analyses on an electronic voltage transformer's failure by its resonance with very fast transient overvoltage and suppression显示文摘As voltage measuring devices are widely used in the high voltage power system with a primary-secondary-fusion structure,electronic voltage transformers are directly connected to the primary conductor and would face much more serious electromagnetic environments than general secondary equipment.As a result,they would still experience failures even when general protection measures are adopted to suppress overvoltages'amplitudes.To address this issue,an innovative method is proposed after analyses are conducted on the resonance between a transformer and an overvoltage.Within this method,an air-cored coil is installed in a transformer to artificially shift its natural frequency and to dodge the high-frequency dominant component of a transient overvoltage,avoiding the aforementioned resonance and suppressing the secondary overvoltage.In addition,simulations and laboratory tests are conducted to prove this method's validity. | Ruoyu Han Houda Zhu Qing Chen Hongbin Li Yue Tong Linshan Han Yang Jiao | 2024 | High Voltage2024，9，1： | 0 |
| 4 | Deregulation of c-myc and SV40Tag causing brain tumor in mice显示文摘Deregulated expressions of both c-myc and simian virus 40 large T antigen (SV40Tag) are consistent features of lots of tumors. To investigate whether the expression of c-myc and SV40Tag in mouse might help develop a model of human tumor, we generated c-myc transgenics by inserting human c-myc gene into pTRE2 of Tet-On system. We obtained conditional expression of SV40Tag transgenics by the Tet-On system from Yangzhou University. Crossing the c-myc transgenic mouse with the SV40Tag transgenic mice to generate bitransgenics we got double-transgenic mice expressing c-myc and SV40Tag by the Tet-On system. After being treated with doxycycline continuously, single-transgenic SV40Tag mice developed brain tumor infrequently (3 of 84, 3.6%) with a long onset (185 d on average). In contrast, double-transgenic c-myc/SV40Tag mice developed brain tumor with a short onset (96 days on average) and a 41% brain tumor incidence rate (7 of 17, 41%). This tumor was assumed to be me- dulloblastoma. Our experiments suggest that deregulated expression of c-myc and SV40Tag in brain might generate a mouse model of human brain tumor that recapitulates some features of human medulloblastoma. | wu Hong ZHU Hong ZHANG ChengXiang LI HouDa | 2007 | Chinese Science Bulletin2007，52，24： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员