Journal
NATURE CELL BIOLOGY
Volume 13, Issue 10, Pages 1214-U110Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb2332
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Funding
- National Institute of Child Health and Human Development
- National Institutes of Health [GM051994, F32 GM084660-02]
- W.M. Keck Foundation
- Ellison Foundation [AG-SS-1918-07]
- Department of Defense [W81XWH-08-1-0457, W81XWH-06-1-0140]
- Diabetes and Endocrine Resource Center [5P30DK3252025]
- Diabetes Endocrinology Research Center [DK32520]
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The midbody is a singular organelle formed between daughter cells during cytokinesis and required for their final separation. Midbodies persist in cells long after division as midbody derivatives (MB(d)s), but their fate is unclear. Here we show that MB(d)s are inherited asymmetrically by the daughter cell with the older centrosome. They selectively accumulate in stem cells, induced pluripotent stem cells and potential cancer 'stem cells' in vivo and in vitro. MBd loss accompanies stem-cell differentiation, and involves autophagic degradation mediated by binding of the autophagic receptor NBR1 to the midbody protein CEP55. Differentiating cells and normal dividing cells do not accumulate MB(d)s and possess high autophagic activity. Stem cells and cancer cells accumulate MB(d)s by evading autophagosome encapsulation and exhibit low autophagic activity. MBd enrichment enhances reprogramming to induced pluripotent stem cells and increases the in vitro tumorigenicity of cancer cells. These results indicate unexpected roles for MB(d)s in stem cells and cancer 'stem cells'.
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