本综述归纳了近几年来植物中Mut S HOMOLOG1(MSH1)基因的研究进展。根据文献的报道,结合NCBI和Gramene数据库的信息,本综述获得了48个来自于不同植物的完整的MSH1蛋白序列,并对它们进行了系统进化树分析。本综述概述了MSH1基因引发人们...本综述归纳了近几年来植物中Mut S HOMOLOG1(MSH1)基因的研究进展。根据文献的报道,结合NCBI和Gramene数据库的信息,本综述获得了48个来自于不同植物的完整的MSH1蛋白序列,并对它们进行了系统进化树分析。本综述概述了MSH1基因引发人们研究兴趣的三种原因:(1)MSH1是一个在植物中高度保守的核基因,易于克隆和比对,是用来做系统进化树分析的优良候选基因;(2)MHS1基因被干扰之后,能够引起线粒体基因组的改变,进而导致细胞质雄性不育的发生,因此该基因可用于细胞质雄性不育系的创制;(3)MSH1基因被抑制后可以引起DNA甲基化的重新编码,增加表观遗传变异,进而导致表观生长发育优势。这不仅为杂种优势分子机理研究提供了新的方法,而且为遗传育种提供了新的思路。展开更多
As metabolic centers, plant organelles participate in maintenance, defense, and signaling. MSH1 is a plant- specific protein involved in organeUar genome stability in mitochondria and plastids. Plastid depletion of MS...As metabolic centers, plant organelles participate in maintenance, defense, and signaling. MSH1 is a plant- specific protein involved in organeUar genome stability in mitochondria and plastids. Plastid depletion of MSH1 causes heritable, non-genetic changes in development and DNA methylation. We investigated the rash I phenotype using hemi-complementation mutants and transgene-null segregants from RNAi suppres- sion lines to sub-compartmentalize MSH1 effects. We show that MSH1 expression is spatially regulated, specifically localizing to plastids within the epidermis and vascular parenchyma. The protein binds DNA and localizes to plastid and mitochondrial nucleoids, but fractionation and protein-protein interactions data indicate that MSH1 also associates with the thylakoid membrane. Plastid MSH1 depletion results in variegation, abiotic stress tolerance, variable growth rate, and delayed maturity. Depletion from mitochon- dria results in 7%-10% of plants altered in leaf morphology, heat tolerance, and mitochondrlal genome sta- bility. MSH1 does not localize within the nucleus directly, but plastid depletion produces non-genetic changes in flowering time, maturation, and growth rate that are heritable independent of MSH 1. MSH1 deple- tion alters non-photoactive redox behavior in plastids and a sub-set of mitochondrially altered lines. Ectopic expression produces deleterious effects, underlining its strict expression control. Unraveling the complexity of the MSH1 effect offers insight into triggers of plant-specific, transgenerational adaptation behaviors.展开更多
目的:探讨芍药苷调控MLH1和MSH2蛋白增强黑色素瘤细胞放疗敏感性的机制。方法:体外培养构建放疗抵抗性的黑色素瘤M14细胞株(M14-RR); Western blot实验检测M14和M148-RR细胞中MLH1和MSH2的表达水平,MTT细胞实验检测不同浓度的芍药苷对...目的:探讨芍药苷调控MLH1和MSH2蛋白增强黑色素瘤细胞放疗敏感性的机制。方法:体外培养构建放疗抵抗性的黑色素瘤M14细胞株(M14-RR); Western blot实验检测M14和M148-RR细胞中MLH1和MSH2的表达水平,MTT细胞实验检测不同浓度的芍药苷对黑色素瘤细胞活性的影响; Western blot检测芍药苷对黑色素瘤细胞中MLH1和MSH2蛋白水平的影响;免疫荧光检测黑色素瘤细胞γ-H2AX聚集点的情况及对放疗的敏感性; CCK-8实验检测M14-RR细胞株接受放疗后凋亡率和细胞周期的变化。结果:成功构建M14-RR放疗抵抗细胞株后,Western blot检测M14-RR细胞中MLH1和MSH1的表达水平高于M14细胞,MTT细胞实验检测250μg/ml浓度的芍药苷药物对M14细胞最佳抑制率为(63. 61±3. 65)%; Western blot检测250μg/ml浓度的芍药苷组黑色素瘤细胞中MLH1和MSH2的表达水平比对照组细胞的增高[(85. 31±5. 16) vs (38. 26±3. 16),P<0. 05;(74. 15±6. 08) vs (29. 62±3. 57),P<0. 05];免疫荧光检测芍药苷作用黑色素瘤细胞后γ-H2AX聚集点的表达明显增多,DNA损伤增多;芍药苷作用黑色素瘤细胞接受放疗后细胞凋亡率增加,提高黑色素瘤细胞在G1期和S期的分布率,干扰细胞增殖的进程。结论:芍药苷通过调控MLH1和MSH1蛋白增强黑色素瘤细胞的DNA损伤及修复能力,增强其对放疗的敏感性。展开更多
文摘本综述归纳了近几年来植物中Mut S HOMOLOG1(MSH1)基因的研究进展。根据文献的报道,结合NCBI和Gramene数据库的信息,本综述获得了48个来自于不同植物的完整的MSH1蛋白序列,并对它们进行了系统进化树分析。本综述概述了MSH1基因引发人们研究兴趣的三种原因:(1)MSH1是一个在植物中高度保守的核基因,易于克隆和比对,是用来做系统进化树分析的优良候选基因;(2)MHS1基因被干扰之后,能够引起线粒体基因组的改变,进而导致细胞质雄性不育的发生,因此该基因可用于细胞质雄性不育系的创制;(3)MSH1基因被抑制后可以引起DNA甲基化的重新编码,增加表观遗传变异,进而导致表观生长发育优势。这不仅为杂种优势分子机理研究提供了新的方法,而且为遗传育种提供了新的思路。
文摘As metabolic centers, plant organelles participate in maintenance, defense, and signaling. MSH1 is a plant- specific protein involved in organeUar genome stability in mitochondria and plastids. Plastid depletion of MSH1 causes heritable, non-genetic changes in development and DNA methylation. We investigated the rash I phenotype using hemi-complementation mutants and transgene-null segregants from RNAi suppres- sion lines to sub-compartmentalize MSH1 effects. We show that MSH1 expression is spatially regulated, specifically localizing to plastids within the epidermis and vascular parenchyma. The protein binds DNA and localizes to plastid and mitochondrial nucleoids, but fractionation and protein-protein interactions data indicate that MSH1 also associates with the thylakoid membrane. Plastid MSH1 depletion results in variegation, abiotic stress tolerance, variable growth rate, and delayed maturity. Depletion from mitochon- dria results in 7%-10% of plants altered in leaf morphology, heat tolerance, and mitochondrlal genome sta- bility. MSH1 does not localize within the nucleus directly, but plastid depletion produces non-genetic changes in flowering time, maturation, and growth rate that are heritable independent of MSH 1. MSH1 deple- tion alters non-photoactive redox behavior in plastids and a sub-set of mitochondrially altered lines. Ectopic expression produces deleterious effects, underlining its strict expression control. Unraveling the complexity of the MSH1 effect offers insight into triggers of plant-specific, transgenerational adaptation behaviors.
文摘目的:探讨芍药苷调控MLH1和MSH2蛋白增强黑色素瘤细胞放疗敏感性的机制。方法:体外培养构建放疗抵抗性的黑色素瘤M14细胞株(M14-RR); Western blot实验检测M14和M148-RR细胞中MLH1和MSH2的表达水平,MTT细胞实验检测不同浓度的芍药苷对黑色素瘤细胞活性的影响; Western blot检测芍药苷对黑色素瘤细胞中MLH1和MSH2蛋白水平的影响;免疫荧光检测黑色素瘤细胞γ-H2AX聚集点的情况及对放疗的敏感性; CCK-8实验检测M14-RR细胞株接受放疗后凋亡率和细胞周期的变化。结果:成功构建M14-RR放疗抵抗细胞株后,Western blot检测M14-RR细胞中MLH1和MSH1的表达水平高于M14细胞,MTT细胞实验检测250μg/ml浓度的芍药苷药物对M14细胞最佳抑制率为(63. 61±3. 65)%; Western blot检测250μg/ml浓度的芍药苷组黑色素瘤细胞中MLH1和MSH2的表达水平比对照组细胞的增高[(85. 31±5. 16) vs (38. 26±3. 16),P<0. 05;(74. 15±6. 08) vs (29. 62±3. 57),P<0. 05];免疫荧光检测芍药苷作用黑色素瘤细胞后γ-H2AX聚集点的表达明显增多,DNA损伤增多;芍药苷作用黑色素瘤细胞接受放疗后细胞凋亡率增加,提高黑色素瘤细胞在G1期和S期的分布率,干扰细胞增殖的进程。结论:芍药苷通过调控MLH1和MSH1蛋白增强黑色素瘤细胞的DNA损伤及修复能力,增强其对放疗的敏感性。
