f Germination triggers of Metarhizium anisopliae conidia are related to host species
- Authors: RAYMOND J. ST LEGER, MICHAEL J. BIDOCHKA, DONALD W. ROBERTS
- Author for correspondence: Raymond J. St Leger. Tel. + 1 607 254 1252. Fax: + 1 607 254 1242.
- Microbiology, July 1994 140: 1651-1660, doi: 10.1099/13500872-140-7-1651
- Subject: Plant-Microbe Interactions
- Published Online:
The role of selectable strain variations in the development of pathogen strategies was examined using lines of Metarhizium anisopliae isolated from homopteran (isolate 549) or coleopteran (isolate 808) hosts. Conidia of strain 549 germinated in either alanine, glucose, cyclic AMP or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). The non-metabolizable glucose analogues, 3-O-methylglucose and 6-deoxyglucose, did not allow germination by themselves but stimulated germination when added to IBMX. By contrast, 2-deoxyglucose (dGlc) blocked germination on glucose or IBMX and inhibited hyphal growth on other carbon sources including alanine and glycerol. Conidia of strain 808 germinated rapidly in alanine but responded slowly to glucose or IBMX in the medium and were resistant to the growth inhibitory effects of dGIc. Radioactive dGIc was taken up by conidia of strains 549 and 808 at similar rates and was recovered mainly as 2-deoxyglucose 6-phosphate. Competition experiments utilizing both strains demonstrated that glucose, dGIc and 3-O-methylglucose were transported by the same system. Fructose was much less able than glucose to inhibit uptake of dGIc indicating that fructose is taken up by a different transport system than that for glucose. It is unlikely, therefore, that the resistance of strain 808 to dGIc is explained by reduced sugar transport compared with strain 549 but that strains 549 and 808 differ in the regulation of carbon metabolism with some systems in strain 808 showing resistance to the catabolite-repressing effects of glucose. Apparently, catabolite repression is subdivided into different segments as glucose inhibited the derepression of a number of catabolite repressible enzymes in strain 808, including the pathogenicity determinant protease Pr1. The same effect was produced by dGIc but not by 3-O-methylglucose, indicating that the trigger for catabolite repression occurs at the level of transport-associated glucose phosphorylation. A comparative study of 26 isolates indicated that most lines from coleopteran hosts were dGIc resistant and germinated poorly on glucose. Conversely, isolates germinating well on glucose (mostly from hemipteran and lepidopteran hosts) were dGIc susceptible.
© Society for General Microbiology 1994 | Published by the Microbiology Society
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