Genetic control of infection-related development in Magnaporthe oryzae Guotian Li 1,2 , Xiaoying Zhou 2 and Jin-Rong Xu 1,2 Diseases caused by various pathogenic fungi pose a serious threat to global food security. Despite their differences in life cycles, fungal pathogens use well-conserved genetic mechanisms to regulate different developmental and infection processes. This review focuses on the key signaling pathways and recent advances in Magnaporthe oryzae, which is a model for studying fungal–plant interactions. In addition to the core components, a number of upstream genes and downstream targets of the cAMP–PKA and mitogen-activated protein (MAP) pathways have been identified. Recent advances in studies with cytoskeleton organization, effector biology, and ROS signaling in M. oryzae and future directions also are discussed. Addresses 1 Purdue-NWAFU Joint Research Center, College of Plant Protection, Northwest A&F University, Yangling, Shaanxi 712100, China 2 Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN 47907, USA Corresponding author: Xu, Jin-Rong (jinrong@purdue.edu) Current Opinion in Microbiology 2012, 15:678–684 This review comes from a themed issue on Growth and development: eukaryotes Edited by Nicholas J Talbot For a complete overview see the Issue and the Editorial Available online 19th October 2012 1369-5274/$ – see front matter, # 2012 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.mib.2012.09.004 Introduction Fungal pathogens normally initiate infection by attaching dispersing propagules to plant surfaces. In the rice blast fungus Magnaporthe oryzae, a model for studying fungal– plant interactions, specialized infection structures called appressoria are formed at the tip of germ tubes. Turgor pressure generated in melanized appressoria is used to puncture through plant cuticle and cell wall. After penetration, invasive hyphae grow biotrophically in host cells. In late infection stages, infectious growth of the pathogen results in plant cell death and lesion develop- ment [1,2]. In the past two decades, various genetic mechanisms regulating different infection processes have been characterized in M. oryzae. cAMP signaling regulates surface recognition and pathogenesis The cyclic AMP-protein kinase A (cAMP-PKA) pathway is known to regulate morphogenesis and pathogenesis in a number of fungal pathogens (Table 1) [3]. In M. oryzae, appressorium formation requires the attachment of germ tubes to hydrophobic surfaces but can be induced with cAMP or cutin monomers on hydrophilic surfaces. Mol- ecular characterization of the MAC1 adenylate cyclase and CPKA catalytic subunit of PKA genes (Figure 1) further confirmed the role of cAMP signaling in surface recog- nition [1]. Recently, the CAP1 gene was shown to be involved in association with the actin cytoskeleton and Mac1 activation [4]. Several components of heterotrimeric G-proteins, including Ga MagA or MagB, Gb Mgb1, and Gg Mgg1, that function upstream from the cAMP–PKA pathway also have been characterized [5]. Furthermore, Rgs1 (Regulator of G-protein signaling) negatively regulates MagA-dependent adenylate cyclase activity. The rgs1 mutant had an elevated intracellular cAMP level and formed appressoria on hydrophilic surfaces [6], which was similar to the phenotype of mutants deleted of the PDEH cAMP phosphodiesterase gene [7]. Among seven additional RGS-like genes recently characterized in M. oryzae, three of them, RGS3, RGS4, and RGS7, also were required for full virulence [8]. PTH11 encodes a putative G-protein-coupled receptor (GPCR). The defects of pth11 mutants in appressorium formation and pathogenesis were restored by cAMP or DAG treatment, indicating that Pth11 may function as a receptor for cAMP signaling [9]. Transcription factors that may function downstream from the cAMP–PKA pathway in M. oryzae include Mstu1, Som1, and Cdtf1. The mstu1 mutant was reduced in appressorium formation and virulence. It was delayed in the mobilization of lipid bodies and glycogens to appressoria, which is regulated by cAMP signaling [10]. Som1 and Cdtf1 are two novel transcription factors important for sporulation and appressorium formation [11  ]. Som1 interacted strongly with Mstu1 and Cdtf1 but weakly with CpkA in yeast two-hybrid assays. The expression levels of SOM1 and CDTF1 was reduced in both mac1 and cpkA mutants. Pth12 also may be function- ally related to cAMP signaling because exogenous cAMP induced appressorium formation in the pth12 mutant [12]. A well-conserved MAP kinase (MAPK) pathway is required for appressorium formation Although cAMP signaling controls surface recognition, late stages of appressorium formation are regulated by Pmk1, a MAPK orthologous to yeast Fus3/Kss1. The pmk1 deletion mutant failed to form appressoria but still recognized hydrophobic surfaces. Several upstream Available online at www.sciencedirect.com Current Opinion in Microbiology 2012, 15:678–684 www.sciencedirect.com