Abstract Apple Valsa canker (AVC), a disease instigated by Valsa mali (syn. Cytospora mali), poses a significant global threat to apple cultivation. Throughout its infection process, V. mali introduces an array of effector proteins into the host cells aimed at undermining the host immune defenses. The exact molecular mechanisms through which these effectors manipulate host transcription factors (TFs) to promote pathogenesis are not fully understood. This study identifies a ribonuclease T2-like effector, VmRnt2, that notably inhibits INF1-triggered cell death, chitin-induced reactive oxygen species (ROS) bursts, and callose deposition. Knockout of the VmRnt2 gene markedly reduced the virulence of V. mali, without impacting fungal growth or spore production. Conversely, heterologous expression of VmRnt2 in Nicotiana benthamiana and apple markedly enhanced susceptibility to infections by Sclerotinia sclerotiorum and V. mali, respectively, highlighting its pivotal role in facilitating pathogenicity. VmRnt2 was found to interact specifically with an apple TF, MdMYB44, which belongs to the myeloblastosis (MYB) family of proteins. Further functional assays revealed that overexpression of MdMYB44 in apple enhances resistance to V. mali. Additionally, MdMYB44 was shown to bind specifically to the promoter of the defense-related gene MdPR1A, subsequently activating its transcription. Importantly, during V. mali infection, VmRnt2 disrupts the DNA-binding activity of MdMYB44. Collectively, our results elucidate how V. mali employs VmRnt2 to compromise MdMYB44-mediated immune regulation, thereby facilitating the pathogen’s colonization of apple trees.
Liu et al. (Thu,) studied this question.