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P‐body‐induced inactivation of let‐7a miRNP prevents the death of growth factor‐deprived neuronal cells
Author(s) -
Patranabis Somi,
Bhattacharyya Suvendra Nath
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201700633r
Subject(s) - microbiology and biotechnology , ectopic expression , programmed cell death , translation (biology) , biology , cytoplasm , nerve growth factor , apoptosis , rna , growth factor , chemistry , messenger rna , gene , biochemistry , receptor
RNA processing bodies (P‐bodies) are cytoplasmic RNA granules in eukaryotic cells that regulate gene expression by executing the translation suppression and degradation of mRNAs that are targeted to these bodies. P‐bodies can also serve as storage sites for translationally repressed mRNAs both in mammalian cells and yeast cells. In this report, a unique role of mammalian P‐bodies is documented. Depletion of P‐body components dedifferentiate nerve growth factor‐treated PC12 cells, whereas ectopic expression of P‐body components induces the neuronal differentiation of precursor cells. Trophic factor withdrawal from differentiated cells induces a decrease in cellular P‐body size and numbers that are coupled with dedifferentiation and cell death. Here, we report how the expression of P‐body proteins—by ensuring the phosphorylation of argonaute protein 2 and the subsequent inactivation let‐7a miRNPs—prevents the apoptotic death of growth factor‐depleted neuronal cells.—Patranabis, S., Bhattacharyya, S. N. P‐body‐induced inactivation of let‐7a miRNP prevents the death of growth factor‐deprived neuronal cells. FASEB J. 32,1493‐1509 (2018). www.fasebj.org