Physcomitrium (Physcomitrella) patens infection by Colleto-trichum gloeosporioides: understanding the fungal-bryophyte interaction by microscopy, phenomics and RNA sequencing

Anthracnose caused by the hemibiotroph fungi Colletotrichum gloeosporioides is a devastating plant disease with extensive impact on plant productivity. The process of colonization and disease pro-gression of C. gloeosporioides has been studied in a number of angiosperm crops. To better under-stand the evolution of the plant response to pathogens the study of this complex interaction has been extended to bryophytes. The model moss Physcomitrium patens (former Physcomitrella patens) is sensitive to known bacterial and fungal phytopathogens, including C. gloeosporioides, that cause infection and cell death. P. patens responses to these microorganisms resemble that of the angio-sperms. However, the molecular events during the interaction of P. patens and C. gloeosporioides have not been explored. In this work we present a comprehensive approach using microscopy, phenomics and RNA-seq analysis to explore the defense response of P. patens to C. gloeosporioides. Microscopy analysis showed appressoria are already formed at 24 hours after infection (hai) and tissue colonization and cell death occur at since 24 hai and is massive at 48 hai. Consequently, the phenomic analysis showed progressing browning of moss tissues and impaired photosynthesis from 24 to 48 hai. The transcriptomic analysis shows that more than 1,200 P. patens genes were differ-entially expressed in response to Colletotrichum infection. The analysis of differentially expressed gene function showed that the C. gloeosporioides infection led to a transcription reprogramming in P. patens which upregulated genes related with pathogen recognition, secondary metabolism, cell wall reinforcement and regulation of gene expression. In accordance to observed phenomic results some photosynthesis and chloroplast genes were repressed, indicating that under attack P. patens changes its transcription from primary metabolism to defend itself from the pathogen.