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Asymmetric damage segregation at cell division via protein aggregate fusion and attachment to organelles

Coelho, Miguel; Tolić, Iva Marija (2015) Asymmetric damage segregation at cell division via protein aggregate fusion and attachment to organelles. BioEssays, 37 (7). pp. 740-747. ISSN 0265-9247

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The segregation of damaged components at cell division determines the survival and aging of cells. In cells that divide asymmetrically, such as Saccharomyces cerevisiae, aggregated proteins are retained by the mother cell. Yet, where and how aggregation occurs is not known. Recent work by Zhou and collaborators shows that the birth of protein aggregates, under specific stress conditions, requires active translation, and occurs mainly at the endoplasmic reticulum. Later, aggregates move to the mitochondrial surface through fis1-dependent associa- tion. During replicative aging, aggregate association with the mother-cell mitochondria contributes to the asym- metric segregation of aggregates, because mitochondria in the daughter cell do not carry aggregates. With increasing age of mother cells, aggregates lose their connection to the mitochondria, and segregation is less asymmetric. Relating these findings to other mechanisms of aggregate segregation in different organisms, we postulate that fusion between aggregates and their tethering to organelles such as the vacuole, nucleus, ER, or mitochondria are common principles that establish asymmetric segregation during stress resistance and aging.

Item Type: Article
Uncontrolled Keywords: Asymmetric segregation; Endoplasmic reticulum; Fusion; Mitochondria; Organelle tethering; Partitioning; Protein aggregates; Retention; Sequestration
Subjects: NATURAL SCIENCES > Biology > Biochemistry and Molecular Biology
Divisions: Division of Molecular Biology
Depositing User: Patrik Risteski
Date Deposited: 26 Oct 2015 07:50
DOI: 10.1002/bies.201400224

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