| Summary: | <p>Abstract</p> <p>Background</p> <p>In order to initiate plant infection, fungal spores must germinate and penetrate into the host plant. Many fungal species differentiate specialized infection structures called appressoria on the host surface, which are essential for successful pathogenic development. In the model plant pathogen <it>Magnaporthe grisea </it>completion of mitosis and autophagy cell death of the spore are necessary for appressoria-mediated plant infection; blocking of mitosis prevents appressoria formation, and prevention of autophagy cell death results in non-functional appressoria.</p> <p>Results</p> <p>We found that in the closely related plant pathogen <it>Colletotrichum gloeosporioides</it>, blocking of the cell cycle did not prevent spore germination and appressoria formation. The cell cycle always lagged behind the morphogenetic changes that follow spore germination, including germ tube and appressorium formation, differentiation of the penetrating hypha, and <it>in planta </it>formation of primary hyphae. Nuclear division was arrested following appressorium formation and was resumed in mature appressoria after plant penetration. Unlike in <it>M. grisea</it>, blocking of mitosis had only a marginal effect on appressoria formation; development in hydroxyurea-treated spores continued only for a limited number of cell divisions, but normal numbers of fully developed mature appressoria were formed under conditions that support appressoria formation. Similar results were also observed in other <it>Colletotrichum </it>species. Spores, germ tubes, and appressoria retained intact nuclei and remained viable for several days post plant infection.</p> <p>Conclusion</p> <p>We showed that in <it>C. gloeosporioides </it>the differentiation of infection structures including appressoria precedes mitosis and can occur without nuclear division. This phenomenon was also found to be common in other <it>Colletotrichum </it>species. Spore cell death did not occur during plant infection and the fungus primary infection structures remained viable throughout the infection cycle. Our results show that the control of basic cellular processes such as those coupling cell cycle and morphogenesis during fungal infection can be substantially different between fungal species with similar lifestyles and pathogenic strategies.</p>
|
|---|
