Strains selleck screening library of S. nodorum lacking these genes displayed variety of independent phenotypes during growth in vitro.

One of the most apparent phenotypic defects under normal growth conditions was the complete lack of pycnidia formation or accompanying asexual sporulation. This phenotype is shared by other S. nodorum strains possessing defects in signalling pathways, and as such, was consistent with earlier findings in S. nodorum[9, 11, 13]. Along with growth defects in vitro, the mutant strains also exhibited different abilities to cause disease. Lesion formation on leaves inoculated with strains lacking with Gna1 or Gga1 was delayed but appeared comparable to that of the wild type after two weeks post inoculation. Leaves inoculated with Gba1 though failed to elicit any response from the leaves after 5 dpi, and only a very mild chlorotic response was evident after two weeks. This implies that Gba1 has a critical role in disease development in S. nodorum. Given the almost complete lack of symptom development, it could be suggested that Gba1, like StuA[14], has a role in effector regulation. However this is only speculation and requires

further analysis. Nutrient sensing in the S. nodorum gna1, gba1 and gga1 strains Dramatic growth differences between the mutant strains and the wild-type SN15 were noted on agar plate medium. On V8PDA, SN15 grows radially symmetrical with pycnidia forming in distinct selleck inhibitor circadian bands [15]. The gna1 and gba1 mutant strains both show a similar banding pattern, in mycelial growth, indicating that these strains have not lost the capacity to perceive a light signal. The radial growth of all three

mutant strains 10 dpi was reduced by comparison to SN15 on all tested media. The variation in radial growth of the mutant strains when growing on different carbon sources confirmed that the S. nodorum G-protein(s) play(s) a role in carbon source utilization. In comparison to the wild-type SN15, which displayed a statistically similar radial growth rate when provided with arabinose, fructose, glucose, sucrose or trehalose as a sole carbon source. The comparatively slower growth of gna1 on sucrose was interesting when considering this strain’s Resminostat slower growth on glucose, but significantly higher growth on fructose. Kraakman et al., (1999) showed that the GPCR Gpr1 binds extracellular glucose in the yeast Saccharomyces cerevisiae and stimulates cAMP synthesis through the Gα subunit Gpa2. Likewise Lemaire et al., (2004) showed both glucose and sucrose induced cAMP signalling through the receptor Gpr1, however it was not fructose-induced. Although deletion of either Gpr1 or Gpa2 did not result in a reduced growth rate in S. cerevisiae, the strains in the study were not limited to a Selleckchem Z-DEVD-FMK single carbon source [16].