Literature summary for 3.1.1.31 extracted from

Crimmins, G.T.; Schelle, M.W.; Herskovits, A.A.; Ni, P.P.; Kline, B.C.; Meyer-Morse, N.; Iavarone, A.T.; Portnoy, D.A.
Listeria monocytogenes 6-phosphogluconolactonase mutants induce increased activation of a host cytosolic surveillance pathway (2009), Infect. Immun., 77, 3014-3022.

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Cloned(Commentary)

Cloned (Comment)	Organism
wild-type or pgl mutant expressed in mice	Listeria monocytogenes

Localization

Localization	Comment	Organism	GeneOntology No.	Textmining

Organism

Organism	UniProt	Comment	Textmining
Listeria monocytogenes	-	10403S or 10403S mdrM deletion mutant (DP-L5444) background	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
6-phospho-D-glucono-1,5-lactone + H2O	-	Listeria monocytogenes	6-phospho-D-gluconate	-	?

Synonyms

Synonyms	Comment	Organism
6-phosphogluconolactonase	-	Listeria monocytogenes
PGL	-	Listeria monocytogenes

General Information

General Information	Comment	Organism
malfunction	pgl deletion mutant has decreased growth in glucose-limiting minimal medium but grows normally when excess glucose is added. The Pgl deletion mutant has increased expression of several beta-glucosidases, consistent with inhibition of beta-glucosidases by 6-phosphogluconolactone, it accumulates and secretes a glucose-derived metabolite. Pgl deletion enhances activation of host IFN-beta expression independently of mdrM. At 48 h after infection of mice with 1 50% lethal dose, the pgl deletion mutant exhibits a 15- to 30fold growth defect in the liver and spleen. Pgl deletion mutant is more sensitive to oxidative stress, i.e., to diamide and hydrogen peroxide but not to the antibiotic control	Listeria monocytogenes

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Release 2023.1 (January 2023)