SUMMARY: Spores of 1604 can be induced to germinate by incubation in L-Ala (the ALA pathway) or in a combination of β-D-gIucose (Glc), β-fructose (Fru), L-Asn and K (the GFAK pathway). Biochemical analysis of the germination response of a mutant deficient in the ALA pathway revealed that L-Ala can replace L-Asn in the GFAK pathway (the GFAlaK pathway). In contrast to the ALA pathway of both the wild-type and of a mutant, the GFAlaK pathway w as insensitive to D-Ala and showed the same overall inhibitor profile as the GFAK pathway of wild-type and spores. It is deduced that a second L-Ala receptor with different characteristics to that functioning in the ALA pathway is present in wild-type spores. Analysis of the germination response of a mutant showed that whilst the rate of ALA germination could be stimulated by Glc as well as by Fru in the presence of Glc, the spores could not germinate in GFAK. In addition, Glc and Fru were unable to reverse D-Ala inhibition of L-Ala germination which they do in the wild-type. Thus, in the mutant, the L-Ala/L-Asn receptor in the GFAK pathway is defective. It is concluded that the germination receptors in the ALA and GFAK pathways can functionally interact with each other to initiate spore germination. This conclusion is discussed in relation to proposed models of triggering of spore germination.


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