Summary
Reactive oxygen species (ROS) produced in chloroplasts cause oxidative damage, but also signal to control chloroplast quality control, cell death, and gene expression. The mechanisms behind these pathways remain largely unknown.
The Arabidopsis thaliana plastid ferrochelatase two (fc2) mutant produces the ROS singlet oxygen in chloroplasts that activates such signaling pathways. Here we mapped one fc2 suppressor mutation to CYTIDINE TRIPHOSPHATE SYNTHASE TWO (CTPS2), which encodes one of five enzymes in Arabidopsis necessary for cytoplasmic de novo CTP (and dCTP) synthesis.
The ctps2 mutation blocks singlet oxygen signals by specifically reducing plastid (not mitochondrial) transcripts and DNA content. These phenotypes are restored by exogenous feeding of the dCTP precursor deoxycytidine, suggesting that ctps2 blocks signaling by limiting nucleotides for plastid genome maintenance.
An investigation of CTPS orthologs in Brassicaceae showed that CTPS2 is a member of an ancient lineage distinct from CTPS3. Complementation studies confirmed this analysis; CTPS3 was unable to compensate for CTPS2 function in providing nucleotides for plastid DNA and chloroplast signaling.
Our studies link cytoplasmic nucleotide metabolism with chloroplast quality control pathways. Such a connection is achieved by CTPS enzymes that may have evolved specialized functions in providing nucleotides to specific subcellular compartments.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
Current email addresses: KA: kalamdari{at}email.arizona.edu, KEF: kefisher{at}email.arizona.edu, DWW: dwelsh625{at}email.arizona.edu, SR: snigdharai{at}arizona.edu, KP: kpalos{at}email.arizona.edu, ADLN: an425{at}cornell.edu.