Nuclear mutations in Saccharomyces cerevisiae that affect the escape of DNA from mitochondria to the nucleus.
Nuclear mutations in Saccharomyces cerevisiae that affect the escape of DNA from mitochondria to the nucleus.
复制标题
酿酒酵母的核突变影响 DNA 从线粒体逃逸到细胞核。
DOI：
10.1093/genetics/134.1.21
复制
发表时间：
1993
期刊：
影响因子：
3.3
通讯作者：
Fox,TD
中科院分区：
文献类型：
--
作者：
Thorsness,PE;Fox,TD
我们已经将携带TRP1基因及其相关DNA复制起点ARS1的酵母核DNA片段插入到一株携带染色体trp1缺失的菌株的功能性线粒体染色体中。TRP1在细胞器内不表达。然而，这种Trp-株很容易产生呼吸活性Trp+克隆，该克隆含有TRP1/ARS1片段，与部分线粒体DNA(MtDNA)相关，在它们的核中复制。因此，Trp+克隆是DNA从线粒体逃逸并迁移到细胞核的结果。我们已经分离到21个核突变体，其中mtDNA逃逸速率通过筛选对Trp+的乳头率增加而增加。所有21个突变都是隐性的，并分为6个互补组，称为YME1-YME6。除了增加mtDNA逃逸速度外，yme1突变还导致37度的热敏呼吸缺陷表型和14度的完全葡萄糖培养冷敏生长缺陷。虽然其他yme突变没有检测到生长表型，但在两个双突变组合中观察到了协同作用：一个yme1，yme2双突变在30℃下无法呼吸，一个yme4，yme6双突变在所有测试的温度下都无法呼吸。所有呼吸缺陷都不是由功能性线粒体DNA丢失引起的。这些发现表明，yme1、yme2、yme4和yme6突变改变了线粒体的功能，从而导致DNA从细胞器逃逸的速度增加。
We have inserted a yeast nuclear DNA fragment bearing the TRP1 gene and its associated origin of DNA replication, ARS1, into the functional mitochondrial chromosome of a strain carrying a chromosomal trp1 deletion. TRP1 was not phenotypically expressed within the organelle. However, this Trp- strain readily gave rise to respiratory competent Trp+ clones that contained the TRP1/ARS1 fragment, associated with portions of mitochondrial DNA (mtDNA), replicating in their nuclei. Thus the Trp+ clones arose as a result of DNA escaping from mitochondria and migrating to the nucleus. We have isolated 21 nuclear mutants in which the rate of mtDNA escape is increased by screening for increased rates of papillation to Trp+. All 21 mutations were recessive and fell into six complementation groups, termed YME1-YME6. In addition to increasing the rate of mtDNA escape, yme1 mutations also caused a heat-sensitive respiratory deficient phenotype at 37 degrees and a cold-sensitive growth defect on complete glucose medium at 14 degrees. While the other yme mutations had no detectable growth phenotypes, synergistic interactions were observed in two double mutant combinations: a yme1, yme2 double mutant failed to respire at 30 degrees and a yme4, yme6 double mutant failed to respire at all temperatures tested. None of the respiratory defects were caused by loss of functional mtDNA. These findings suggest that yme1, yme2, yme4 and yme6 mutations alter mitochondrial functions and thereby lead to an increased rate of DNA escape from the organelle.