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中国微生物遗传学研究在2015年取得了重要进展。本文回顾了2015年度中国本土科研团队在微生物遗传学领域取得的若干重要科研进展,扼要介绍了若干重点论文,展示了中国科学家在本领域的学术贡献。在基础微生物遗传学领域,明确了调控基因表达的一系列重要生物大分子的组成、结构和功能,解析了微生物免疫系统识别外源核酸片段的分子基础,阐明了多个微生物来源重要活性物质的生物合成途径及新颖的酶学反应过程,发现了微生物基因表达调控的新机理,在微生物发育、进化与群体行为生物学方面也取得一定进展。在工业微生物遗传学方面,阐明了微生物制造及其分子基础。在病原微生物遗传学方面,研究了多个致病菌的遗传调控,明晰了致病菌-宿主相互作用的遗传机制,在基因组水平解析了微生物耐药、新发病原和环境微生物的遗传机理,为致病菌防控新措施的研发提供了基础。在微生物多样性与环境微生物遗传学方面,展示了利用微生物遗传多样性的特点通过催化获得特定手性的化合物具有较好应用前景,肠道微生物组学研究方兴未艾。 相似文献
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《遗传》杂志是中国科学院主管、中国科学院遗传与发育生物学研究所和中国遗传学会共同主办、科学出版社出版、朱立煌教授主编的全国性学术期刊,中国自然科学核心期刊。主要报道动物遗传与育种、植物遗传与育种、人类与医学遗传、分子与微生物遗传等领域的最新成果与进展。主要栏目有:研究报告、技术与方法、专论与综述、争鸣与讨论、遗传学教学、遗传学史、会议消息及书讯、成果交流及产品介绍等。内容丰富、可读性强,深受生物学相关专业科研人员和大专院校师生的欢迎。2000年以来,《遗传》杂志改为大16开本,页码由48页、64页、80页增至100余页,同时,彩色图版随文印刷,印刷与装订质量不断提高。 相似文献
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对后基因组时代"微生物遗传学"课程教学进行探讨。提出以故事化课堂和形象化讲解增加学生的学习乐趣。为了更好地帮助学生理解后基因组学方法,将后基因组学与微生物遗传学融合教学(包括正向遗传学方法与快速正向遗传学方法、单基因敲除和表型分析与全基因组规模基因敲除和表型分析、传统的遗传相互作用与全基因组的遗传相互作用融合讲授)。此外,生物信息学网络资源的介绍延伸了课堂教学并提高了课堂教学质量。 相似文献
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Hyperglycemia is considered as one of the major determinants in the development of diabetic retinopathy, but the progression of retinopathy resists arrest after hyperglycemia is terminated, suggesting a metabolic memory phenomenon. Diabetes alters the expression of retinal genes, and this continues even after good glycemic control is re‐instituted. Since the expression of genes is affected by chromatin structure that is modulated by post‐translational modifications of histones, our objective is to investigate the role of histone acetylation in the development of diabetic retinopathy, and in the metabolic memory phenomenon. Streptozotocin‐induced rats were maintained either in poor glycemic control (PC, glycated hemoglobin, GHb >11%) or good glycemic control (GC, GHb <6%) for 12 months, or allowed to be in PC for 6 months followed by in GC for 6 months (PC‐GC). On a cellular level, retinal endothelial cells, the target of histopathology of diabetic retinopathy, were incubated in 5 or 20 mM glucose for 4 days. Activities of histone deacetylase (HDAC) and histone acetyltransferase (HAT), and histone acetylation were quantified. Hyperglycemia activated HDAC and increased HDAC1, 2, and 8 gene expressions in the retina and its capillary cells. The activity HAT was compromised and the acetylation of histone H3 was decreased. Termination of hyperglycemia failed to provide any benefits to diabetes‐induced changes in retinal HDAC and HAT, and histone H3 remained subnormal. This suggests “in principle” the role of global acetylation of retinal histone H3 in the development of diabetic retinopathy and in the metabolic memory phenomenon associated with its continued progression. J. Cell. Biochem. 110: 1306–1313, 2010. © 2010 Wiley‐Liss, Inc. 相似文献
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GCN5 is a histone acetyltransferase (HAT) essential for development in mammals and critical to stress responses in yeast. The protozoan parasite Toxoplasma gondii is a serious opportunistic pathogen. The study of epigenetics and gene expression in this ancient eukaryote has pharmacological relevance and may facilitate the understanding of these processes in higher eukaryotes. Here we show that the disruption of T. gondii GCN5 yields viable parasites, which were subsequently employed in a proteomics study to identify gene products affected by its loss. Promoter analysis of these TgGCN5-dependent genes, which were mostly parasite specific, reveals a conserved T-rich element. The loss of TgGCN5 does not attenuate virulence in an in vivo mouse model. We also discovered that T. gondii is the only invertebrate reported to date possessing a second GCN5 (TgGCN5-B). TgGCN5-B harbors a strikingly divergent N-terminal domain required for nuclear localization. Despite high homology between the HAT domains, the two TgGCN5s exhibit differing substrate specificities. In contrast to TgGCN5-A, which exclusively targets lysine 18 of H3, TgGCN5-B acetylates multiple lysines in the H3 tail. We also identify two ADA2 homologues that interact differently with the TgGCN5s. TgGCN5-B has the potential to compensate for TgGCN5-A, which probably arose from a gene duplication unique to T. gondii. Our work reveals an unexpected complexity in the GCN5 machinery of this primitive eukaryote. 相似文献