CIA5 (CCM1) notes — Chlamydomonas reinhardtii, UniProt Q9FED4

Deep research

2026-10-03: scripts/deep_research_wrapper.py CHLRE CIA5 falcon --fallback perplexity-lite
run once. Falcon returned HTTP 402 Payment Required; the perplexity-lite fallback
failed because the perplexity provider is not available in this environment. Not
retried. No deep-research file exists; the review is built from the cached primary
literature below.

The GOA file for Q9FED4 has a header only: no existing GO annotations. All
annotations in the review are NEW proposals.
UniProt entry is unreviewed (TrEMBL, "CCM1-A"), only Gene3D "Classic Zinc Finger"
and MobiDB disorder regions. Gene model CHLRE_02g096300v5.

Cloned independently as Ccm1 and Cia5 in back-to-back PNAS papers.
PMID:11287669
cia5 lesion is His54 in the zinc finger. PMID:11287669
Two zinc sites, each binding 1 Zn. PMID:18202004; C2H2 finger at
~35-70 PMID:42448334.
Complex of 290-580 kDa PMID:18202004.
Volvox ortholog, 51% identity, conserved zinc region, putative NLS/NES, C-terminal
LXXLL PMID:21253860. Lineage-restricted PMID:42488443.

mRNA and protein constitutive in high and low CO2 PMID:11309511; therefore thought to be activated
post-translationally PMID:22634760.
C-terminal 54-aa truncation complements but causes constitutive expression of
CO2-responsive genes PMID:11309511.
Degraded by proteasome under Zn deficiency PMID:42448334.

Nuclear: CCM1-mGold in ccm1-1 PMID:41637450.
Earlier report (Wang et al. 2005, Can J Bot; not in PubMed) cited by PMID:42448334.

CBP1 = ZNG3 (Cre16.g684650), CobW/WW-domain COG0523 GTPase, constitutive nuclear
partner. Shimamura 2026 PMID:41637450 calls it CBP1 and shows it represses 27 of
41 CCM1-dependent genes under high CO2; Kusi-Appiah 2026 PMID:42448334 calls it
ZNG3, shows proteasomal co-degradation in low Zn.
GDH1/2 co-purify more weakly PMID:41637450.

Almost all LCI genes require CCM1 PMID:15235119. ~25% of transcriptome affected by
CIA5 and/or CO2 PMID:22634760. Includes HLA3, LCIA, LCIB, LCIC, CAH1, CAH3, LCR1
[PMID:22634760, PMID:42488443], LHCSR3 and PSBS PMID:37031262, and the pyrenoid
kinase KEY1 PMID:42488443.

PMID:22634760 (2012): sequences recognized by the "putative DNA binding domain"
unknown.
PMID:41637450 (2026 PNAS): "direct DNA binding has not been demonstrated, suggesting
that CCM1 operates in conjunction with other nuclear factors."
PMID:42488443 (2026 review): cites Chen and Spalding 2026 (Plant Mol Biol Rep,
doi:10.1007/s11105-025-01670-7) — RBSS + gel shift with purified full-length CIA5,
GC-rich 9-bp motif (GGGGCGGGG per publisher abstract found by web search) in
promoters of three CIA5-dependent genes. Not indexed in PubMed; publisher page not
retrievable here, so not cached and not used as direct evidence.
Decision: do NOT assert GO:0003700 DNA-binding transcription factor activity or
GO:0043565 sequence-specific DNA binding. A single in vitro study, unavailable for
verification, with no in vivo occupancy data. Recorded as a suggested question.
Positive regulation of DNA-templated transcription (GO:0045893, IMP) is proposed,
because the effect is transcriptional and CIA5 is a nuclear regulator whose own
C-terminal state determines target transcription PMID:11309511.

The stimulus is CO2 limitation. GO has no "low CO2" term; GO:0071244 is the
closest. Comparator check (QuickGO, exact, experimental): Candida RCA1, UME6, FLO8
and yeast CST6 (transcription regulators mediating CO2 responses) carry GO:0071244 or
GO:0010037 by IMP, so annotating a CO2-responsive transcription regulator to this
term follows existing practice. CIA5 passes the participation test as the regulator
that converts CO2 status into transcriptional output.
Module modules/pyrenoid_ccm.yaml assertion (no MF, process GO:0071244) is
supported.