PPGR - Gene Detail

Basic Information

Gene ID	SESE_070322.g View in Genome Browser
Position	Scaffold_332052:34221705-34231951 (+) 10246bp
Gene Type	gene
Gene Description (Protein Product)	Excises uracil residues from the DNA which can arise as a result of misincorporation of dUMP residues by DNA polymerase or due to deamination of cytosine
Organism	Sequoia sempervirens
Also AS	AT3G18630

upstream:

Domain

Database	EntryID	E-Value	Start	end	InterPro ID	Description

Regulation&Interaction

Protein-protein interaction (PPI)

SESE_071043.g N-glycosylase DNA lyase

SESE_070447.g Structure-specific nuclease with 5'-flap endonuclease and 5'-3' exonuclease activities involved in DNA replication and repair. During DNA replication, cleaves the 5'-overhanging flap structure that is generated by displacement synthesis when DNA polymerase encounters the 5'-end of a downstream Okazaki fragment. It enters the flap from the 5'-end and then tracks to cleave the flap base, leaving a nick for ligation. Also involved in the long patch base excision repair (LP-BER) pathway, by cleaving within the apurinic apyrimidinic (AP) site-terminated flap. Acts as a genome stabilization factor that prevents flaps from equilibrating into structurs that lead to duplications and deletions. Also possesses 5'-3' exonuclease activity on nicked or gapped double- stranded DNA, and exhibits RNase H activity. Also involved in replication and repair of rDNA and in repairing mitochondrial DNA

SESE_072467.g DNA damage-binding protein

Regulatory gene

SESE_007476.g dof zinc finger protein

SESE_022567.g dof zinc finger protein

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Annotation

Orthologous Group

Orthologous ID	Species Number	All hits in PereRegDB	Hits of this species	Orthologous Detail

Pathway

GO Term	Description	GO Category
GO:0003674	molecular_function	MF
GO:0003824	catalytic activity	MF
GO:0004844	uracil DNA N-glycosylase activity	MF
GO:0005575	cellular_component	CC
GO:0005622	intracellular anatomical structure	CC
GO:0005623	obsolete cell	CC
GO:0005737	cytoplasm	CC
GO:0005739	mitochondrion	CC
GO:0006139	nucleobase-containing compound metabolic process	BP
GO:0006259	DNA metabolic process	BP
GO:0006281	DNA repair	BP
GO:0006284	base-excision repair	BP
GO:0006285	base-excision repair, AP site formation	BP
GO:0006725	cellular aromatic compound metabolic process	BP
GO:0006807	nitrogen compound metabolic process	BP
GO:0006950	response to stress	BP
GO:0006974	cellular response to DNA damage stimulus	BP
GO:0008150	biological_process	BP
GO:0008152	metabolic process	BP
GO:0009987	cellular process	BP
GO:0016787	hydrolase activity	MF
GO:0016798	hydrolase activity, acting on glycosyl bonds	MF
GO:0016799	hydrolase activity, hydrolyzing N-glycosyl compounds	MF
GO:0019104	DNA N-glycosylase activity	MF
GO:0033554	cellular response to stress	BP
GO:0034641	cellular nitrogen compound metabolic process	BP
GO:0043170	macromolecule metabolic process	BP
GO:0043226	organelle	CC
GO:0043227	membrane-bounded organelle	CC
GO:0043229	intracellular organelle	CC
GO:0043231	intracellular membrane-bounded organelle	CC
GO:0044237	cellular metabolic process	BP
GO:0044238	primary metabolic process	BP
GO:0044260	cellular macromolecule metabolic process	BP
GO:0044424	obsolete intracellular part	CC
GO:0044444	obsolete cytoplasmic part	CC
GO:0044464	obsolete cell part	CC
GO:0046483	heterocycle metabolic process	BP
GO:0050896	response to stimulus	BP
GO:0051716	cellular response to stimulus	BP
GO:0071704	organic substance metabolic process	BP
GO:0090304	nucleic acid metabolic process	BP
GO:0097506	deaminated base DNA N-glycosylase activity	MF
GO:0097510	base-excision repair, AP site formation via deaminated base removal	BP
GO:0140097	catalytic activity, acting on DNA	MF
GO:1901360	organic cyclic compound metabolic process	BP

KEGG Term	Name	Description
map03410	Base excision repair	Base excision repair (BER) is the predominant DNA damage repair pathway for the processing of small base lesions, derived from oxidation and alkylation damages. BER is normally defined as DNA repair initiated by lesion-specific DNA glycosylases and completed by either of the two sub-pathways: short-patch BER where only one nucleotide is replaced and long-patch BER where 2-13 nucleotides are replaced. Each sub-pathway of BER relies on the formation of protein complexes that assemble at the site of the DNA lesion and facilitate repair in a coordinated fashion. This process of complex formation appears to provide an increase in specificity and efficiency to the BER pathway, thereby facilitating the maintenance of genome integrity by preventing the accumulation of highly toxic repair intermediates.