Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.26.3 (
RNase III
)
1,015
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Antisense long noncoding (aslnc)RNAs are extensively degraded by the nuclear exosome and the cytoplasmic exoribonuclease Xrn1 in the budding yeast
Saccharomyces cerevisiae
, lacking RNAi. Whether the
ribonuclease III
Dicer affects aslncRNAs in close RNAi-capable relatives remains unknown. Using genome-wide RNA profiling, here we show that aslncRNAs are primarily targeted by the exosome and Xrn1 in the RNAi-capable budding yeast
Naumovozyma castellii
, Dicer only affecting Xrn1-sensitive aslncRNAs levels in Xrn1-deficient cells. The
dcr1
and
xrn1
mutants display synergic growth defects, indicating that Dicer becomes critical in the absence of Xrn1. Small RNA sequencing showed that Dicer processes aslncRNAs into small RNAs, with a preference for Xrn1-sensitive aslncRNAs. Consistently, Dicer localizes into the cytoplasm. Finally, we observed an expansion of the exosome-sensitive antisense transcriptome in
N. castellii
compared with
S. cerevisiae
, suggesting that the presence of cytoplasmic RNAi has reinforced the nuclear RNA surveillance machinery to temper aslncRNAs expression. Our data provide fundamental insights into aslncRNAs metabolism and open perspectives into the possible evolutionary contribution of RNAi in shaping the aslncRNAs transcriptome.
Life Sci
Alliance
2019 10
PMID:Endogenous RNAi pathway evolutionarily shapes the destiny of the antisense lncRNAs transcriptome. 3146