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PCTM1_ECOLX
ID   PCTM1_ECOLX             Reviewed;         185 AA.
AC   P0DV25;
DT   25-MAY-2022, integrated into UniProtKB/Swiss-Prot.
DT   25-MAY-2022, sequence version 1.
DT   03-AUG-2022, entry version 2.
DE   RecName: Full=Pycsar effector protein EcPycTM;
DE            Short=EcPycTM {ECO:0000303|PubMed:34644530};
GN   Name=pycTM {ECO:0000303|PubMed:34644530}; ORFNames=Ga0132381_1286;
OS   Escherichia coli.
OC   Bacteria; Proteobacteria; Gammaproteobacteria; Enterobacterales;
OC   Enterobacteriaceae; Escherichia.
OX   NCBI_TaxID=562;
RN   [1]
RP   NUCLEOTIDE SEQUENCE [LARGE SCALE GENOMIC DNA].
RC   STRAIN=E831;
RA   Hur Y.J.;
RL   Submitted (AUG-2015) to the EMBL/GenBank/DDBJ databases.
RN   [2]
RP   FUNCTION, ANTIVIRAL DEFENSE, AND CLASSIFICATION.
RC   STRAIN=E831;
RX   PubMed=34644530; DOI=10.1016/j.cell.2021.09.031;
RA   Tal N., Morehouse B.R., Millman A., Stokar-Avihail A., Avraham C.,
RA   Fedorenko T., Yirmiya E., Herbst E., Brandis A., Mehlman T.,
RA   Oppenheimer-Shaanan Y., Keszei A.F.A., Shao S., Amitai G., Kranzusch P.J.,
RA   Sorek R.;
RT   "Cyclic CMP and cyclic UMP mediate bacterial immunity against phages.";
RL   Cell 0:0-0(2021).
CC   -!- FUNCTION: Pycsar (pyrimidine cyclase system for antiphage resistance)
CC       provides immunity against bacteriophage. The pyrimidine cyclase (PycC)
CC       synthesizes cyclic nucleotides in response to infection; these serve as
CC       specific second messenger signals. The signals activate the adjacent
CC       effector, leading to bacterial cell death and abortive phage infection.
CC       A clade E Pycsar system. {ECO:0000269|PubMed:34644530}.
CC   -!- FUNCTION: The effector component of a two-gene Pycsar system.
CC       Expression of this and adjacent cytidylate cyclase EcPycC (AC P0DV24)
CC       confers resistance to bacteriophage P1 and T5; this protein is required
CC       for resistance. When cells expressing the Pycsar system are infected by
CC       phage T5 at low multiplicity of infection (0.2 MOI) the culture
CC       survives, at 2.0 MOI bacteria enter growth arrest. The same cells enter
CC       growth arrest after exposure to 250 uM cCMP but not cUMP; this effector
CC       protein responds only to cCMP, usually produced by its cognate NTP
CC       cyclase. Some of the cells treated with cCMP have abnormal membrane
CC       protrusions, probably due to effects on membrane integrity.
CC       {ECO:0000269|PubMed:34644530}.
CC   -!- SUBCELLULAR LOCATION: Cell inner membrane {ECO:0000305}; Multi-pass
CC       membrane protein {ECO:0000255}.
CC   -!- MISCELLANEOUS: T5 phage that escape Pycsar have mutated major capsid
CC       protein pb8 (D20, AC Q6QGD8); infection with these phage elicits less
CC       cCMP production. Ectopic expression of the capsid protein in addition
CC       to both Pycsar genes does not induce effector-mediated toxicity,
CC       suggesting another factor is necessary. {ECO:0000269|PubMed:34644530}.
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DR   EMBL; CXXA01000028; -; NOT_ANNOTATED_CDS; Genomic_DNA.
DR   GO; GO:0016021; C:integral component of membrane; IEA:UniProtKB-KW.
DR   GO; GO:0005886; C:plasma membrane; IEA:UniProtKB-SubCell.
DR   GO; GO:0000166; F:nucleotide binding; IEA:UniProtKB-KW.
DR   GO; GO:0051607; P:defense response to virus; IEA:UniProtKB-KW.
PE   3: Inferred from homology;
KW   Antiviral defense; Cell inner membrane; Cell membrane; Membrane;
KW   Nucleotide-binding; Transmembrane; Transmembrane helix.
FT   CHAIN           1..185
FT                   /note="Pycsar effector protein EcPycTM"
FT                   /id="PRO_0000455230"
FT   TRANSMEM        32..52
FT                   /note="Helical"
FT                   /evidence="ECO:0000255"
FT   TRANSMEM        63..83
FT                   /note="Helical"
FT                   /evidence="ECO:0000255"
FT   TRANSMEM        141..161
FT                   /note="Helical"
FT                   /evidence="ECO:0000255"
SQ   SEQUENCE   185 AA;  21141 MW;  570E0D9E7B242AB7 CRC64;
     MEIEKNKEKI KLQFDIIKRT DGYISTTNNK AALLLAVNGA TATILSNKVG YFAGLFHENC
     LYMVIFFLLL FMISIFIFMS VLLSLKSIIP NMRGVKEKWD STDSNVSFVY ISSNNDGKNY
     YKKYLMESED GLLLDMCEQS FILSCIAKQK FLFFSSAVSW IKRAYACIIV LVIFKFVDYV
     NGALL
 
 
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