| Rice blast,caused by the filamentous ascomycete fungus Magnaporthe oryzae,is a serious disease to rice and other crops.M.oryzae produces asexual spores named conidia,which contact with the host surface and sense a suitable environmental signal,to differentiate into a dome-shaped cell named appressorium for assisting host infection.In this process,protein acetylation catalyzed by histone acetylase or deacetylase plays an important regulatory role,including induction of autophagy to promote asexual sporulation,regulation of cellular transcription to adapt to oxygen stress adversity during infection and so on.Light is one of the most important environmental signals to regulate disease outbreaks,and can regulate many physiological activities of fungi,including growth and development,pathogenicity and so on.However,the underlying mechanism of light-regulation on M.oryzae pathogenesis is not fully understood.At present,research of M.oryzae photoreceptor is mainly focused on the blue light receptor WC-1.The role of other photoreceptors in M.oryzae photomorphogenesis and/or pathogenicity has not been reported.Two blue-light receptor encoding genes were identified in this study,namely Mo WC-2and Mo CRY-1.Using PEG-mediated protoplast transformation,gene deletion and genetic complementation strains of Mo WC-2 and Mo CRY-1 were generated,and verified by antibiotics-resistance screening,PCR and Southern blot analysis.The mutants were then analyzed for growth,conidiation and infection phenotypes.The results showed that the△ mowc-2 mutant completely lost the photoperiod banding,and reduced in conidiation and pathogenicity.These results indicated that Mo WC-2 may not only participate in conidia formation and pathogenicity,but also be the core element or regulator of circadian clock of M.oryzae.The △mocry-1 mutant displayed reduced sporulation,while it was significantlymore pathogenic than wild-type conidia in either dark or light conditions.Light suppressed disease lesion formation caused by the wild-type conidia on barley leaves,which is called light-dependent disease suppression.However,such light-dependent disease suppression was not prominent in the △ mocry-1 mutant,indicating a role played by Mo CRY-1 in lightperception and/or response,which may regulate M.oryzae pathogenicity.The results of q RT-PCR showed that the expression levels of Mo WC-2 and Mo CRY-1 genes were significantly up-regulated under light condiation compared to that in the dark,which further proved that these two genes were involved in light-dependent regulation of M.oryzae pathogenicity.On the other hand,we identified a gene encoding a histone deacetylase of M.oryzae,which is orthologous to rice Os HDAC1.We nameed it as Mo RPD3.Mo Rpd3 is a catalytic component of a class I histone deacetylation complex HDAC1.In this study,we obtained the Mo RPD3 overexpression mutants OXRPD3.Phenotypic analysis showed that when Mo RPD3 was overexpressed,the vegetative growth of M.oryzae was not affected,while conidia formation was increased significantly,the conidial germination rate was increased,the infective hyphae was decreased,and the pathogenicity was reduced significantly.These results indicated that Mo RPD3 may regulate conidia formation and germination,as well as invasive growth of infetous hyphae,thus critical for M.oryzae pathogenicity.Overexpressed GFP-Mo Rpd3 was seen to localize in the nucleus and cytoplasm in vegetative hyphae.In summary,we have shown that the blue-light receptor Mo Wc-2 regulates growth and pathogenic development of M.oryzae,likely through regulation of its circadian rhythm.The blue-light receptor Mo Cry-1 responds to light signals,and is involved in lightdependent disease suppression in Magnaporthe oryzae.The histone deacetylase Mo Rpd3 regulates the sporulation,germination and pathogenic differentiation of M.oryzae. |
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