Engulfment pathways promote programmed cell death by enhancing the unequal segregation of apoptotic potential
Sayantan Chakraborty,
Eric J. Lambie,
Samik Bindu,
Tamara Mikeladze-Dvali and
Barbara Conradt ()
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Sayantan Chakraborty: Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried
Eric J. Lambie: Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried
Samik Bindu: Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried
Tamara Mikeladze-Dvali: Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried
Barbara Conradt: Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried
Nature Communications, 2015, vol. 6, issue 1, 1-9
Abstract:
Abstract Components of the conserved engulfment pathways promote programmed cell death in Caenorhabditis elegans (C. elegans) through an unknown mechanism. Here we report that the phagocytic receptor CED-1 mEGF10 is required for the formation of a dorsal–ventral gradient of CED-3 caspase activity within the mother of a cell programmed to die and an increase in the level of CED-3 protein within its dying daughter. Furthermore, CED-1 becomes enriched on plasma membrane regions of neighbouring cells that appose the dorsal side of the mother, which later forms the dying daughter. Therefore, we propose that components of the engulfment pathways promote programmed cell death by enhancing the polar localization of apoptotic factors in mothers of cells programmed to die and the unequal segregation of apoptotic potential into dying and surviving daughters. Our findings reveal a novel function of the engulfment pathways and provide a better understanding of how apoptosis is initiated during C. elegans development.
Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms10126
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DOI: 10.1038/ncomms10126
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