Cells resist starvation through nutrients dependent splice switch
Removing introns from coding genes through the process of splicing is a ubiquitous feature of all eukaryotes. Here we show that global remodeling of splicing program through changing the stoichiometry of spliceosomal components is a key mediator of cell resistance to starvation. Transcriptomic and genetic analyses indicate that nutrients depletion reconfigures the splicing program to favor the splicing of meiotic genes and repress ribosomal protein genes by asymmetrically increasing the abundance of U1 small nuclear protein complex. Impairing U1 binding to splice site alters the nutrients dependent changes in the splicing program leading to increased sensitivity to starvation. This work reveals a new mechanism by which cells resist starvation through changes in the stoichiometry of the spliceosomal components and reprograming of the spliceosome splicing preference. Overall design: To compare splicing genome wide using WT, nam8 deletion, and mud1 mutant strains in both log phase growth and nutrient depeletion/starvation conditions. This was done using Multiplexed Primer Extension Sequencing