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Simultaneous activation of Tor and suppression of ribosome biogenesis by TRIM-NHL proteins promotes terminal differentiation.

Published version
Peer-reviewed

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Type

Article

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Authors

Gui, Jinghua 
Grobicki, Katarina ZA 
Teixeira, Felipe Karam  ORCID logo  https://orcid.org/0000-0001-7651-1657

Abstract

Tissue development and homeostasis depend on the balance between growth and terminal differentiation, but the mechanisms coordinating these processes remain elusive. Accumulating evidence indicates that ribosome biogenesis (RiBi) and protein synthesis, two cellular processes sustaining growth, are tightly regulated and yet can be uncoupled during stem cell differentiation. Using the Drosophila adult female germline stem cell and larval neuroblast systems, we show that Mei-P26 and Brat, two Drosophila TRIM-NHL paralogs, are responsible for uncoupling RiBi and protein synthesis during differentiation. In differentiating cells, Mei-P26 and Brat activate the target of rapamycin (Tor) kinase to promote translation, while concomitantly repressing RiBi. Depletion of Mei-P26 or Brat results in defective terminal differentiation, which can be rescued by ectopic activation of Tor together with suppression of RiBi. Our results indicate that uncoupling RiBi and translation activities by TRIM-NHL activity creates the conditions required for terminal differentiation.

Description

Keywords

CP: Developmental biology, brain, cyst, fruit fly, metabolism, nucleolus, ovary, proliferation, stem cell, translation, tumour, Animals, Drosophila Proteins, Tripartite Motif Proteins, Drosophila, Cell Differentiation, Ribosomes, DNA-Binding Proteins

Journal Title

Cell Rep

Conference Name

Journal ISSN

2211-1247
2211-1247

Volume Title

Publisher

Elsevier BV
Sponsorship
Wellcome Trust (206257/Z/17/Z)
Human Frontier Science Program (HFSP) (CDA00032/2018-C)
Human Frontier Science Program
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2023-10-23 14:37:29
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2023-02-08 00:30:48
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