Open AccessRHEB-mTOR axis regulates expression of transposonsTf2s in fission yeast.
Author(s) -
Yukiko Nakase,
Tomohiro Matsumoto
Publication year - 2018
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.221457
Subject(s) - biology , yeast , rheb , fission , transposable element , pi3k/akt/mtor pathway , schizosaccharomyces pombe , genetics , microbiology and biotechnology , saccharomyces cerevisiae , signal transduction , gene , genome , mtorc1 , physics , quantum mechanics , neutron
Human TSC2 gene, predisposing to a disease, Tuberous sclerosis complex (TSC), encodes a GTPase-activating protein for RHEB GTPase. Loss of TSC2 results in constitutive activation of RHEB and its target mTOR. We previously reported that fission yeast retrotransposons, Tf2s were abnormally induced upon nitrogen starvation in cells lacking tsc2+ gene (Δtsc2), a homolog of human TSC2 gene, and a dominant active mutant of fission yeast RHEB GTPase (rhb1-DA4). We report here that induction of Tf2s in these mutants is suppressed by overexpression of the cgs2+ gene encoding a cAMP-specific phosphodiesterase, or deletion of components in the glucose/cAMP signaling pathway, namely Cyr1, Pka1, Tor1 and a stress-activated transcription factor Atf1. The results suggest that the glucose/cAMP signaling pathway is down-regulated when cells are starved for nitrogen. We also show that Tf2s are degraded via autophagy, which is under control of Tor2, a homolog of human mTOR. It appears that failure in the two processes, downregulation of the glucose/cAMP signaling pathway and induction of autophagy, allows abnormal induction of Tf2s upon nitrogen starvation in Δtsc2 and rhb1-DA4.