2013 Fiscal Year Final Research Report
A Mechanism for Mitochondrial DNA Copy Number-regulated Simultaneous Expression of Proteins in Respiratory Complexes.
| Project/Area Number |
23510237
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Genome biology
|
|---|
| Research Institution | The Institute of Physical and Chemical Research |
|---|
Principal Investigator |
LING Feng 独立行政法人理化学研究所, 吉田化学遺伝学研究室, 専任研究員 (70281665)
|
|---|
| Project Period (FY) |
2011 – 2013
|
| Keywords | 出芽酵母 / DNA組換え / ミトコンドリアDNA / ミトコンドリア融合 / 酸化ストレス応答 / ローリングサークル型複製 / DNA損傷 / Mhr1タンク質 |
|---|
| Research Abstract |
We found that mitochondrial fusion induces dissociation of Complex V of the respiratory chain and ROS generation, which increases mitochondrial DNA (mtDNA) copy number in a manner dependent on the homologous DNA pairing protein Mhr1 and also increases in the mtDNA-encoded subunits of Complex V. These results suggested that activation of recombination-dependent replication during mitochondrial fusion plays important roles in maintenance of mitochondrial genomes by preventing generation of mitochondria lacking mtDNA. We further uncovered a mechanism in which relative expression levels of the DNA damage inducible protein Din7 to Mhr1 determine the choice of replication or repair after pairing of homologous DNA by Mhr1.
|
