Abstract：
:Mitochondria are dynamic organelles that have been linked to stem cell homeostasis. However, the mechanisms involved in mitochondrial regulation of stem cell fate determination remain elusive. Here we discover that epithelial-mesenchymal transition (EMT), a key process in cancer progression, induces mitochondrial fusion through regulation of the miR200c-PGC1α-MFN1 pathway. EMT-activated MFN1 forms a complex with PKCζ and is required for PKCζ-mediated NUMB phosphorylation and dissociation from the cortical membrane to direct asymmetric division of mammary stem cells, where fused mitochondria are tethered by MFN1-PKCζ to the cortical membrane and asymmetrically segregated to the stem cell-like progeny with enhanced glutathione synthesis and reactive oxygen species scavenging capacities, allowing sustaining of a self-renewing stem cell pool. Suppression of MFN1 expression leads to equal distribution of the fragmented mitochondria in both progenies that undergo symmetric luminal cell differentiation. Together, this study elucidates an essential role of mitofusin in stem cell fate determination to mediate EMT-associated stemness.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Wu MJ,Chen YS,Kim MR,Chang CC,Gampala S,Zhang Y,Wang Y,Chang CY,Yang JY,Chang CJdoi
10.1016/j.cmet.2018.11.004subject
Has Abstractpub_date
2019-04-02 00:00:00pages
993-1002.e6issue
4eissn
1550-4131issn
1932-7420pii
S1550-4131(18)30681-8journal_volume
29pub_type
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