Clostridium perfringens spore germination: characterization of germinants and their receptors.
Clostridium perfringens food poisoning is caused by type A isolates carrying a chromosomal enterotoxin (cpe) gene (C-cpe), while C. perfringens-associated non-food-borne gastrointestinal (GI) diseases are caused by isolates carrying a plasmid-borne cpe gene (P-cpe). C. perfringens spores are thought to be the important infectious cell morphotype, and after inoculation into a suitable host, these spores must germinate and return to active growth to cause GI disease. We have found differences in the germination of spores of C-cpe and P-cpe isolates in that (i) while a mixture of L-asparagine and KCl was a good germinant for spores of C-cpe and P-cpe isolates, KCl and, to a lesser extent, L-asparagine triggered spore germination in C-cpe isolates only; and (ii) L-alanine or L-valine induced significant germination of spores of P-cpe but not C-cpe isolates. Spores of a gerK mutant of a C-cpe isolate in which two of the proteins of a spore nutrient germinant receptor were absent germinated slower than wild-type spores with KCl, did not germinate with L-asparagine, and germinated poorly compared to wild-type spores with the nonnutrient germinants dodecylamine and a 1:1 chelate of Ca2+ and dipicolinic acid. In contrast, spores of a gerAA mutant of a C-cpe isolate that lacked another component of a nutrient germinant receptor germinated at the same rate as that of wild-type spores with high concentrations of KCl, although they germinated slightly slower with a lower KCl concentration, suggesting an auxiliary role for GerAA in C. perfringens spore germination. In sum, this study identified nutrient germinants for spores of both C-cpe and P-cpe isolates of C. perfringens and provided evidence that proteins encoded by the gerK operon are required for both nutrient-induced and non-nutrient-induced spore germination.
Paredes-Sabja
Daniel
D
Department of Biomedical Sciences, Oregon State University, Corvallis, OR 97331, USA.
Torres
J Antonio
JA
Setlow
Peter
P
Sarker
Mahfuzur R
MR
D000409:Alanine / Q000378:metabolism / Q000494:pharmacology; D001216:Asparagine / Q000378:metabolism / Q000494:pharmacology; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D002876:Chromosomes, Bacterial / Q000235:genetics; D003016:Clostridium perfringens / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects; D005798:Genes, Bacterial; D008957:Models, Genetic; D009154:Mutation; D009876:Operon / Q000235:genetics; D010957:Plasmids / Q000235:genetics; D011189:Potassium Chloride / Q000378:metabolism / Q000494:pharmacology; D011522:Protons; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013171:Spores, Bacterial / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D013696:Temperature; D014633:Valine / Q000378:metabolism / Q000494:pharmacology
D001426:Bacterial Proteins; D011522:Protons; D011189:Potassium Chloride; D001216:Asparagine; D014633:Valine; D000409:Alanine