Introns are mediators of cell response to starvation.
5' Untranslated Regions
/ genetics
Cell Respiration
Culture Media
/ pharmacology
Cyclic AMP-Dependent Protein Kinases
/ metabolism
Food Deprivation
Gene Expression Regulation, Fungal
Introns
/ genetics
Mechanistic Target of Rapamycin Complex 1
/ metabolism
Microbial Viability
/ drug effects
Nutrients
/ deficiency
Protein Biosynthesis
Ribosomal Proteins
/ genetics
Ribosomes
/ genetics
Saccharomyces cerevisiae
/ cytology
Sequence Deletion
/ genetics
Signal Transduction
Transcriptome
/ genetics
Journal
Nature
ISSN: 1476-4687
Titre abrégé: Nature
Pays: England
ID NLM: 0410462
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
received:
23
02
2018
accepted:
07
12
2018
pubmed:
18
1
2019
medline:
20
6
2019
entrez:
18
1
2019
Statut:
ppublish
Résumé
Introns are ubiquitous features of all eukaryotic cells. Introns need to be removed from nascent messenger RNA through the process of splicing to produce functional proteins. Here we show that the physical presence of introns in the genome promotes cell survival under starvation conditions. A systematic deletion set of all known introns in budding yeast genes indicates that, in most cases, cells with an intron deletion are impaired when nutrients are depleted. This effect of introns on growth is not linked to the expression of the host gene, and was reproduced even when translation of the host mRNA was blocked. Transcriptomic and genetic analyses indicate that introns promote resistance to starvation by enhancing the repression of ribosomal protein genes that are downstream of the nutrient-sensing TORC1 and PKA pathways. Our results reveal functions of introns that may help to explain their evolutionary preservation in genes, and uncover regulatory mechanisms of cell adaptations to starvation.
Identifiants
pubmed: 30651641
doi: 10.1038/s41586-018-0859-7
pii: 10.1038/s41586-018-0859-7
doi:
Substances chimiques
5' Untranslated Regions
0
Culture Media
0
Ribosomal Proteins
0
Mechanistic Target of Rapamycin Complex 1
EC 2.7.11.1
Cyclic AMP-Dependent Protein Kinases
EC 2.7.11.11
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
612-617Commentaires et corrections
Type : CommentIn