In:
PLOS Biology, Public Library of Science (PLoS), Vol. 21, No. 9 ( 2023-9-18), p. e3002310-
Abstract:
Decline of mitochondrial function is a hallmark of cellular aging. To counteract this process, some cells inherit mitochondria asymmetrically to rejuvenate daughter cells. The molecular mechanisms that control this process are poorly understood. Here, we made use of matrix-targeted D-amino acid oxidase (Su9-DAO) to selectively trigger oxidative damage in yeast mitochondria. We observed that dysfunctional mitochondria become fusion-incompetent and immotile. Lack of bud-directed movements is caused by defective recruitment of the myosin motor, Myo2. Intriguingly, intact mitochondria that are present in the same cell continue to move into the bud, establishing that quality control occurs directly at the level of the organelle in the mother. The selection of healthy organelles for inheritance no longer works in the absence of the mitochondrial Myo2 adapter protein Mmr1. Together, our data suggest a mechanism in which the combination of blocked fusion and loss of motor protein ensures that damaged mitochondria are retained in the mother cell to ensure rejuvenation of the bud.
Type of Medium:
Online Resource
ISSN:
1545-7885
DOI:
10.1371/journal.pbio.3002310
DOI:
10.1371/journal.pbio.3002310.g001
DOI:
10.1371/journal.pbio.3002310.g002
DOI:
10.1371/journal.pbio.3002310.g003
DOI:
10.1371/journal.pbio.3002310.g004
DOI:
10.1371/journal.pbio.3002310.g005
DOI:
10.1371/journal.pbio.3002310.g006
DOI:
10.1371/journal.pbio.3002310.g007
DOI:
10.1371/journal.pbio.3002310.g008
DOI:
10.1371/journal.pbio.3002310.g009
DOI:
10.1371/journal.pbio.3002310.s001
DOI:
10.1371/journal.pbio.3002310.s002
DOI:
10.1371/journal.pbio.3002310.s003
DOI:
10.1371/journal.pbio.3002310.s004
DOI:
10.1371/journal.pbio.3002310.s005
DOI:
10.1371/journal.pbio.3002310.s006
DOI:
10.1371/journal.pbio.3002310.s007
DOI:
10.1371/journal.pbio.3002310.s008
DOI:
10.1371/journal.pbio.3002310.s009
DOI:
10.1371/journal.pbio.3002310.s010
DOI:
10.1371/journal.pbio.3002310.s011
DOI:
10.1371/journal.pbio.3002310.s012
DOI:
10.1371/journal.pbio.3002310.s013
DOI:
10.1371/journal.pbio.3002310.s014
DOI:
10.1371/journal.pbio.3002310.s015
DOI:
10.1371/journal.pbio.3002310.s016
DOI:
10.1371/journal.pbio.3002310.s017
DOI:
10.1371/journal.pbio.3002310.s018
DOI:
10.1371/journal.pbio.3002310.s019
DOI:
10.1371/journal.pbio.3002310.r001
DOI:
10.1371/journal.pbio.3002310.r002
DOI:
10.1371/journal.pbio.3002310.r003
DOI:
10.1371/journal.pbio.3002310.r004
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2023
detail.hit.zdb_id:
2126773-X
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