Once aerial conidia have adhered to the host cuticle, they can
germinate when the right conditions are met. These conditions
include favorable temperature and humidity, and the presence of
an exogenous carbon source (Bidochka et al., 2000). Germinated
conidia grow germ tubes, that develop into a penetration peg that
perforates the cuticle to invade the host. Little is known about
genes that are involved in host sensing and regulating the differentiation
of penetration pegs. In some strains, it was reported that
germlings differentiate into appressoria, although the formation
of an appressorium structure is not required for a successful infection
(Wagner and Lewis, 2000). In B. bassiana strain Bb0062, the
MAP kinase gene Bbmpk1 was shown to be required for appressorium
formation and penetration on cicada wings (Zhang et al.,
2010). Also, the disruption of the MAP kinase gene Bbhog1 resulted
in reduced frequency of appressorium formation and reduced
virulence (Zhang et al., 2009). MAP kinases affect a number of
processes in entomopathogenic fungi, including conidial adhesion(step 1), appressorium formation and virulence. Regulators, such MAP kinases, affect the expression of several downstream genes,
and their disruption has pleiotropic effects. Such studies therefore do not elucidate which target genes are specifically involved in appressorium formation. More targeted studies are required to unravel how appressoria (if they are formed) contribute to virulence.