The Magnaporthe grisea species complex and plant pathogenesis

Summary

Taxonomy

Kingdom Fungi; Phylum Ascomycota; Class Sordariomycetes; Order Magnaporthales; Family Pyriculariaceae (anamorph)/Magnaporthaceae (teleomorph); Genus Pyricularia (anamorph)/Magnaporthe (teleomorph); Species P. grisea (anamorph)/M. grisea (teleomorph).

Host range

Very broad at the species level, including rice, wheat, barley, millet and other species of the Poaceae (Gramineae).

Disease symptoms

Can be found on all parts of the plant, including leaves, leaf collars, necks, panicles, pedicels, seeds and even the roots. Initial symptoms are white to grey–green lesions or spots with darker borders, whereas older lesions are elliptical or spindle‐shaped and whitish to grey with necrotic borders. Lesions may enlarge and coalesce to eventually destroy the entire leaf.

Disease control

Includes cultural strategies, genetic resistance and the application of chemical fungicides.

Geographical distribution

Widespread throughout the rice‐growing regions of the globe and has been reported in more than 85 countries.

Genomic structure

Different isolates possess similar genomic sizes and overall genomic structures. For the laboratory strain 70‐15: assembly size, 40.98 Mb; number of chromosomes, seven; number of predicted genes, 13 032; G + C composition, 51.6%; average gene contains 451.6 amino acids; mitochondrion genome size, 34.87 kb.

Useful website

http://www.broadinstitute.org/annotation/genome/magnaporthe_comparative/MultiHome.html.

Introduction

Rice (Oryza sativa) is the most important food crop around the world, contributing to 30% of the global caloric intake (Gnanamanickam, 2009). Outbreaks of rice blast are a constant threat to cereal production worldwide, which could result in an annual loss of rice sufficient to feed more than 60 million people (Choi et al., 2013). The causal agent of rice blast is the heterothallic ascomycete Magnaporthe oryzae (asexual state: Pyricularia oryzae), which was previously known as Magnaporthe grisea. Magnaporthe oryzae is a haploid filamentous ascomycete and causes blast disease on a broad range of grasses, including rice and other species of the Poaceae (Ou, 1985). Strains isolated from Digitaria (e.g. crabgrass and finger‐grass) have been defined as M. grisea, whereas isolates from rice and other hosts have been named M. oryzae (Klaubauf et al., 2014). The separation of these two groups is based on distinct genetic differences and the lack of interbreeding capacity. Recently, a phylogenetic analysis conducted by Luo et al. (2015) has demonstrated that M. oryzae and M. grisea are distinct from other isolates of the order Magnaporthales with the ability to infect host aerial parts using appressoria. Tosa and Chuma (2014) established a perfect correspondence between anamorphs and teleomorphs of M. oryzae and M. grisea, and proposed that the Magnaporthales isolate group, composed of M. oryzae, M. grisea and at least two cryptic species indistinguishable in conidial morphology (Hirata et al., 2007), should be regarded as the M. grisea species complex. Rice blast, also known as grey leaf spot in grasses, is one of the most destructive diseases of rice (Borromeo et al., 1993; Valent, 1990). During the disease cycle, the fungus initially produces three‐celled pyriform conidia which spread from plant to plant, germinate on the host leaf surface and form appressoria at the end of the germ tubes (Bourett and Howard, 1991). The mature appressoria subsequently form penetration pegs that break through the plant cuticle, allowing the fungus to enter into and manifest within the host plant cells (Howard and Valent, 1996; Howard et al., 1991). Following successful penetration, the infectious hyphae spread quickly and cause lesions over the entire leaves. Within 7 days, the lesions exhibit numerous conidia that can initiate a new disease cycle (Talbot et al., 1996) (Figure 1). The breeding of resistant cultivars of rice has been developed as one of the strategies to combat blast; however, M. oryzae can rapidly evolve to overcome host resistance (Ou, 1980; Zeigler et al., 1994). A full understanding of the molecular basis of the pathogenicity of M. oryzae and its interaction with the host is instrumental for the development of novel environmentally sound strategies to manage blast disease and to protect world food supplies. In addition, M. oryzae has several advantages that make it an ideal model organism for the study of plant‐pathogenic fungi and their interactions with hosts (Dean et al., 2005). For example, it can be cultured on defined medium and has a well‐established transformation system, facilitating biochemical and molecular analyses, it has a relatively small genome and already has extensive genetic mapping data available, and a draft sequence of the host (rice) genome is also complete. Here, we review the nomenclature and phylogenetic relationship of the Magnaporthe complex, the genome sequence of the M. oryzae isolates, advances in our understanding of infection‐related developmental events and the roles of effectors during the host–pathogen interaction.

Figure 1.

Field symptoms of neck blast and the rice blast disease cycle. (A) In the field, neck and panicle blast are major causes of rice yield losses. The fungus sporulates profusely at nodes on the rice stem and rots the neck of the mature rice plant, causing loss of the panicle or preventing grain filling and maturation. The photograph was taken from a rice blast outbreak that occurred in October 2014 in Jiangsu Province, China. (B) The rice blast fungus causes lesions through asexual spores and initiates a new disease cycle within 7 days.

Nomenclature of the M. Grisea Complex

According to the latest information, there are a total of 137 Poaceae members known as hosts of blast fungi (http://nt.ars-grin.gov/fungaldatabases/, updated on 6 April 2012) (Farr and Rossman, 2009). The heterothallic ascomycete M. grisea (Hebert) Barr [anamorph: Pyricularia grisea (Cook) Sacc.] is pathogenic to rice and a number of other grass genera, causing blast, one of the most destructive diseases of rice, and grey leaf spot of grasses (Borromeo et al., 1993; Valent, 1990). Blast is also the most important disease of rice as a result of its widespread global occurrence. Rice blast results in significant destruction under conducive conditions, accounting for 11%–15% annual yield losses (Baker et al., 1997). Magnaporthe grisea, which has been reported to infect more than 50 grass species (Ou, 1987), was first isolated from crabgrass (Digitaria sanguinalis) and named P. grisea (Saccardo, 1880). The name P. oryzae was also used to describe the fungus when Cavara identified it from rice in 1892 (Cavara, Fungi Longobardiae #49). Although slight morphological differences were noted between these two descriptions, the difference was not sufficient to differentiate between the species. Consequently, both names were used synonymously. Even then, Sprague (1950) noted that, despite the difficulty in observing morphological distinctions, rice was predominantly observed to be the host of P. oryzae in the literature available at that time. Following successful mating of the species (Barr, 1977; Yaegashi and Udagawam, 1978), M. grisea was proposed as the name for the M. grisea complex according to the rules of nomenclature (Rossman et al., 1990). However, on the basis of multilocus genealogy and mating experiments, Couch and Kohn (2002) defined M. oryzae as a new species separated from M. grisea. In 2014, Klaubauf et al. reported that a few Magnaporthe‐ and Pyricularia‐like species were unrelated to Magnaporthaceae and Pyriculariaceae. Pyricularia oryzae/P. grisea isolates were clustered into two related clades. In addition, some host plants, such as Eleusine, Oryza, Setaria or Triticum, were exclusively infected by P. oryzae isolates, whereas other host plants, such as Cenchrus, Echinochloa, Lolium, Pennisetum or Zingiber, were infected by different Pyricularia species. This finding shows that host range is not sufficient as a taxonomic criterion and additional and extensive pathotyping is also needed (Klaubauf et al., 2014). The recently issued Article 59.1 of the Melbourne Code considers names for sexual and asexual morphs equally (McNeill et al., 2012). Based on this, Luo and Zhang (2013) suggested that the name P. oryzae should be adopted for the rice blast fungus. As M. oryzae is a widely used name, some researchers have considered keeping the name Magnaporthe for the blast fungus to minimize the inconvenience and possible confusions over issues such as quarantines that a name change could bring. However, this requires an extensive and laborious process, including a change in the type species, as the blast fungus is not congenetic with the type species of Magnaporthe. This issue remains under discussion within the user community.

Divergent Lineage and Phylogenetic Relationship of the M. Grisea Complex

Host range studies have been used to define fundamentally distinct groups within M. grisea (species, populations and clonal lineages). Several host range studies have been performed in either a laboratory or glasshouse, with conflicting results that do not necessarily reflect the host range in nature (Ou, 1987). Subsequently, clonal lineages from O. sativa (field populations) identified by DNA fingerprinting were found to be associated with distinct assemblages of rice cultivars (Borromeo et al., 1993; Correavictoria et al., 1994; Levy et al., 1991, 1993). DNA fingerprinting and restriction fragment length polymorphism (RFLP) studies have not only identified genetically distinct, host‐specific populations of M. grisea (Borromeo et al., 1993; Hamer et al., 1989), but have also resolved highly divergent lineages within M. grisea from Digitaria sp. and O. sativa (Borromeo et al., 1993; Bunting et al., 1996). Borromeo et al. (1993) and Kato et al. (2000) have suggested that the divergent lineages from Digitaria and rice represent distinct species. Further phylogenetic analysis have revealed that M. oryzae and M. grisea are not divergent lineages within the same species, but are independent species. Couch and Kohn (2002) reported that M. oryzae was a new species distinct from M. grisea. They generated the Magnaporthe species gene trees using portions of three conserved genes: actin, β‐tubulin and calmodulin. The results from these gene trees were concordant and delineated two distinct clades within M. grisea. One clade was associated with the grass genus Digitaria and nomenclaturally tied to M. grisea. The other clade was associated with O. sativa and other cultivated grasses, and was described as a new species M. oryzae. Although, to date, no morphological characters can distinguish between the two, M. oryzae and M. grisea are not interfertile. Therefore, M. oryzae is distinguished from M. grisea by several base substitutions in each of three loci, as well as results from mating analysis. In this way, these authors also concluded that M. oryzae is the scientifically correct name for isolates associated with rice blast and grey leaf spot (Couch and Kohn, 2002). Choi et al. (2013) also characterized the phylogenetic diversity within the M. grisea complex. They performed multilocus sequence typing using actin, β‐tubulin and calmodulin gene sequences of isolates from crabgrass, rice and other grasses. A single most‐parsimonious tree (MPT) was generated based on the combined sequences of the three genes or three individual genes. The tree resolved three clades with high bootstrap values. In the MPT, two of the three included phylogenetic species were M. oryzae and M. grisea. The last group, consisting of five isolates from other grasses, was designated the Neo group, which is a phylogenetically distinct species from M. oryzae and M. grisea.

Genome Sequence of the M. Oryzae Isolates

Genomic information helps to promote the understanding of the molecular events leading to fungal pathogenicity and aids in the design of new disease control strategies. In addition, the identification of any genetic variations in fungal pathogens, such as M. oryzae, may foresee whether there are possibilities for the fungus to circumvent otherwise disease‐resistant cultivars. To date, the genome of 53 M. oryzae isolates has been sequenced and is publically available (http://www.ncbi.nlm.nih.gov/assembly/?term=magnaporthe; http://genome. Jouy.inra.fr/gemo). Different isolates possess similar genome sizes and gene numbers (Chen et al., 2013a; Chiapello et al., 2015; Dean et al., 2005; Dong et al., 2015; Xue et al., 2012) (Table 1). These findings indicate that M. oryzae exhibits various degrees of genetic variation among its field isolates.

Table 1.

Genome assembly and annotation statistics of 53 Magnaporthe oryzae isolates.

Strain (Magnaporthe oryzae)	Genome coverage	Size (Mb)	GC (%)	Scaffolds	Contigs	Gene	Protein
70‐15	7×	41.0	51.59	53	216	13032	12836
Y34	21×	38.9	51.30	1198	2114	12862	12860
P131	20×	38.0	51.40	1822	2601	12713	12713
KJ201	199×	45.1	50.70	123	3188	–	–
98‐06	135×	42.3	50.80	284	1161	14019	–
4091‐5‐8	68×	37.5	–	–	8886	–	–
HN19311	5.7×	36.7	51.80	2998	3014	10256	–
FJ81278	34×	37.9	51.40	3518	3783	10453	–
FR13	4×	42.4	–	2051	79619	14384	–
GY11	42×	39.0	–	1964	13188	14781	–
PH14	56×	40.0	–	711	11772	13816	–
TH12	48×	40.1	–	940	9908	14026	–
TH16	53×	39.1		171	4114	13571	–
US71	80×	41.2	–	220	7398	13803	–
BR32	55×	41.9	–	111	6044	14336	–
CD156	50×	42.7	–	237	26535	14067	–
2303.1	65×	38.0	–	–	6787	–	–
1801.4	69×	35.8	–	–	8396	–	–
1106.2	76×	37.6	–	–	5680	–	–
1836.3	78×	35.8	–	–	7899	–	–
4403.2	73×	36.3	–	–	8416	–	–
401.4	80×	36.0	–	–	8275	–	–
903.4	74×	36.2	–	–	8248	–	–
4603.4	64×	37.6	–	–	5947	–	–
HB12	74×	36.7	–	–	7622	–	–
JS25	71×	36.9	–	–	6159	–	–
NX37	78×	35.9	–	–	8518	–	–
SC05	77×	36.7	–	–	8190	–	–
ZJ15	73×	37.5	–	–	6575	–	–
CQ11	72×	36.3	–	–	8541	–	–
AH06	70×	37.0	–	–	6061	–	–
GD22	71×	37.0	–	–	7027	–	–
GX01	70×	36.8	–	–	8371	–	–
HN06	69×	36.1	–	–	7798	–	–
JL10	79×	36.3	–	–	8649	–	–
K84‐01	68×	36.4	–	–	8119	–	–
K88‐24	74×	36.3	–	–	7725	–	–
K91‐13	74×	36.4	–	–	7603	–	–
K91‐30	71×	35.7	–	–	9213	–	–
K96‐07	75×	35.6	–	–	9452	–	–
K88‐07	68×	35.6	–	–	7624	–	–
K91‐10	75×	36.4	–	–	7786	–	–
K93‐16	76×	36.0	–	–	8881	–	–
K96‐11	67×	35.8	–	–	9202	–	–
K98‐10	67×	37.1	–	–	8594	–	–
GOV41	77×	35.9	–	–	8535	–	–
IT10	70×	36.3	–	–	8855	–	–
BM1‐24	67×	36.2	–	–	9429	–	–
CA205	75×	36.0	–	–	9152	–	–
K98‐02	73×	36.0	–	–	9277	–	–
PR72	74×	35.8	–	–	8427	–	–
B157	60×	37.8	–	–	5735	–	–
MG01	60×	39.0	–	–	7722	–	–

–, unknown.

The multiple released genome sequences not only helped to improve the sequence assembly and gene prediction for strain 70‐15, but also provided insights into the mechanisms of genetic variations in pathogen–host interactions. Many specific genes involved in the development and infection process of M. oryzae were identified in different isolates. Specifically, Y34 and P131 contain hundreds of isolate‐specific genes and a number of isolate‐specific duplication events; moreover, each genome contains a large number of poorly conserved transposon‐like elements (Xue et al., 2012). In eight M. oryzae isolates (FR13, PH14, GY11, TH16, TH12, US71, CD156 and BR32) differing in host specificity, the results indicated that the host specificity isolates was associated with a divergence between lineages; adaptation to different hosts, especially to rice, was associated with the presence of a small number of specific gene families (Chiapello et al., 2015). In strain 98‐06, 1.4 Mb of unique genomic sequence was found; a comparison with strain 70‐15 and known pathogenicity‐related genes revealed two critical expression patterns. In addition, a large number of specific effector candidates were identified, and several of these (Iug6, Iug9 and Iug18) were shown to suppress defence responses in rice (Dong et al., 2015). In FJ81278, 1.75 Mb of isolate‐specific genome content carrying 118 novel genes was identified, and 0.83 Mb from HN19311 was also identified. In these two isolates, in total, 256 candidate virulence effectors were identified (Chen et al., 2013a). Further detailed studies of the novel effectors and pathogenicity‐related proteins identified will accelerate our understanding of how the effectors and genomic variation affect the pathogenicity of M. oryzae. Taken together, the results mentioned above indicate that isolate‐unique genes, gene family expansion and the frequent translocation of transposon‐like elements may serve as a source of genetic variability in M. oryzae populations encountering different environments in the field.

Advances in the Infection‐Related Development of M. Oryzae

In recent years, several signal transduction pathways, including the cyclic adenosine monophosphate (cAMP), mitogen‐activated protein kinase (MAPK) and HOG1 signalling pathways, which are involved in surface recognition, appressorium formation, infectious growth, cell wall integrity and osmoregulation, have been characterized in M. oryzae (Li et al., 2012). A number of components of each signalling pathway were identified to have diverse biological or biochemical functions in M. oryzae. Key components of the cAMP pathway, which is important for appressorium differentiation and infection, include regulators of G‐protein signalling RGS (Zhang et al., 2011b), the heterotrimeric G‐protein subunits MagB, Mgb1 and Mgg1 (Liang et al., 2006; Liu and Dean, 1997; Nishimura et al., 2003), adenylate cyclase Mac1 (Choi and Dean, 1997), cyclase‐associated protein Cap1 (Zhou et al., 2012), phosphodiesterase PdeH (Zhang et al., 2011a) and protein kinase A (PKA) catalytic subunit Pka1 (Xu et al., 1997). The MAPK cascade proteins Mst50, Mst11, Mst7 and Pmk1 are also involved in appressorium formation and invasive growth (Park et al., 2006; Xu and Hamer, 1996; Zhao et al., 2005). Mck1, Mkk1 and Mps1 are essential for cell wall integrity, appressorium penetration and virulence (Jeon et al., 2008; Xu et al., 1998; Yin et al., 2015). Sln1, Ssk1, Ssk2 and Osm1, which are major components of the HOG1 pathway, have critical roles in osmoregulation and stress responses (Dixon et al., 1999; Motoyama et al., 2005; Zhang et al., 2010). Furthermore, many downstream transcription factor targets of these pathways have been shown to play pleiotropic roles in M. oryzae, including MoAp1, MoAtf1, MoMsn2, MoSwi6, MoMig1, MoMcm1, MoSfl1, MoMst12, MoMstu1, MoPth12, MoCtdf1 and MoSom1 (Guo et al., 2010, 2011; Li et al., 2011; Mehrabi et al., 2008; Nishimura et al., 2009; Park et al., 2002; Qi et al., 2012; Yan et al., 2011; Zhang et al., 2014; Zhou et al., 2011) (Fig. 2). In addition, a growing number of studies have focused on the regulatory mechanisms of vesicular transport during the development and infection process of M. oryzae. Several soluble N‐ethylmaleimide‐sensitive factor attachment protein receptor (SNARE) proteins, including MoVam7, MoSec22 and MoSso1, which are involved in vesicular transport, have been demonstrated to play pleiotropic roles in M. oryzae (Dou et al., 2011; Giraldo et al., 2013; Song et al., 2010). Although the core components of the signalling or regulatory pathways in fungal pathogens are well conserved and share common functions, it is more important to explore their distinct and specific roles during pathogen development and disease production. It will be interesting and important to identify and characterize new components involved in the signalling and regulatory networks underlying pathogenesis.

Figure 2.

The key signalling pathways involved in infection‐related morphogenesis in Magnaporthe oryzae. A combined model is shown based on those by Li et al. (2012) and Yin et al. (2015).

The Role of M. Oryzae Effectors During the Host–Pathogen Interaction

‘Arms’ races occur constantly between M. oryzae and rice. During the infection process, the biotrophic invasive hyphae of M. oryzae secrete various effectors, involving diverse mechanisms, to facilitate disease development (Oliveira‐Garcia and Valent, 2015). Effectors secreted by M. oryzae can break the first defence line of pathogen‐associated molecular pattern (PAMP)‐triggered immunity (PTI) in rice (Liu et al., 2014), and the avirulence (Avr) effectors are directly or indirectly recognized by cognate R proteins of plants and trigger the second line of defence, termed effector‐triggered immunity (ETI). Nineteen effectors have been characterized from M. oryzae, which include 11 Avr effectors and eight other effectors (Table 2). Among them, two Avr effectors and two other effectors have been identified recently. Several excellent reviews have been published discussing the biology of the identified blast effectors, which are not detailed here. Instead, we elaborate briefly several novel effectors.

Table 2.

Effectors that have been reported in Magnaporthe oryzae.

Name	Accession number	Function	Year	Reference
PWL1	AB480169	Prevents infection of weeping love grass	1995	Kang et al. ( 1995)
PWL2	MGG_04301	Prevents infection of weeping love grass	1995	Sweigard et al. ( 1995)
ACE1	MGG_04428	Recognized by R protein Pi33	2004	Bohnert et al. ( 2004)
Avr‐Pii	AB498874	Recognized by R protein Pii	2009	Lee et al. ( 2009)
AvrPi‐ta	MGG_11081	Recognized by R protein Pi‐ta	2011	Khang et al. ( 2008)
AvrPiz‐t	MGG_18041	Targets host ubiquitination; AVR effector for rice R gene Piz‐t	2012	Park et al. ( 2012)
Avr‐Pik/km/kp	AB498875	Recognized by R protein Pik/km/kp	2012	Kanzaki et al. ( 2012)
MC69	MGG_02848	Required for infection	2012	Saitoh et al. ( 2012)
Slp1	MGG_10097	Chitin oligomer sequestration	2012	Mentlak et al. ( 2012)
Avr1‐CO39	AF463528	Recognized by R protein PiCO39	2012	Ribot et al. ( 2013)
Avr‐Pia	AB498873	Recognized by R protein Pia	2013	Cesari et al. ( 2013)
Bas1	MGG_04795	Accumulates in BIC (Biotrophic Interfacial Complex) and translocates into neighbouring rice cells	2013	Mosquera et al. ( 2009)
Bas2	MGG_09693	Accumulates in BIC and translocates into neighbouring rice cells	2013	Mosquera et al. ( 2009)
Bas3	MGG_11610	Localizes near cell wall crossing points	2013	Mosquera et al. ( 2009)
Bas4	MGG_10914	Outlines growing infectious hyphae	2013	Mosquera et al. ( 2009)
Avr‐Pi9	MGG_12655	Recognized by R protein Pi‐9	2015	Wu et al. ( 2015)
Iug6	KM522919	Targets salicylic acid and ethylene pathways	2015	Dong et al. ( 2015)
Iug9	KM522920	Targets salicylic acid and ethylene pathways	2015	Dong et al. ( 2015)
Avr‐Pib	KM887844	Recognized by R protein Pi‐b	2015	Zhang et al. ( 2015)

Wu et al., 2015 recently identified Avr‐Pi9, corresponding to resistance gene Pi9, by comparative genomics of field isolates (Chen et al., 2013b), whereas another Avr effector, Avr‐Pib, was isolated via map‐based cloning (Zhu et al., 2011). In addition, two novel effectors, Iug6 and Iug9, were explored by genome‐wide transcriptome analysis, which were indicated to suppress rice basal defence by targeting salicylic acid (SA) and ethylene (ET) signalling (Dong et al., 2015). The effectors are generally classified into apoplastic and cytoplasmic effectors according to two distinct effector secretion systems identified in M. oryzae (Giraldo et al., 2013). BIC (Biotrophic Interfacial Complex) is a plant membrane‐rich structure associated with the invasive hyphae of M. oryzae (Khang et al., 2010), at which cytoplasmic effectors, such as Avr‐Pita, Pwl1, Pwl2, Bas2 and Avr‐Piz‐t, accumulate prior to translocation into rice cells via a novel form of secretion involving exocyst components and the Sso1 t‐SNARE (Giraldo et al., 2013). Our latest research has also found that the Qc‐SNARE protein MoSyn8 is involved in the secretion of effectors Avr‐Pia and Avr‐Piz‐t during infection (Qi et al., 2015). However, apoplastic effectors, including Bas4, Avr1‐CO39 and Slp1, are usually dispersed in the extracellular space between the fungal cell wall and the extra‐invasive hyphal membrane (EIHM) (Khang et al., 2010; Zhang and Xu, 2014). All of the identified effectors are putative secreted proteins, except for ACE1, which encodes a hybrid polyketide synthase‐non‐ribosomal peptide synthetase (PKS‐NRPS) (Bohnert et al., 2004). Although effectors of M. oryzae lack conserved motifs, they often share specific or similar expression patterns with high induction during the invasion of plant cells (Fish et al., 2011).

In addition, several fungal secreted effectors can suppress plant innate immunity (Liu et al., 2014). AvrPiz‐t targets the host ubiquitin proteasome system to suppress PTI in rice (Park et al., 2012); Slp1 evades the chitin‐induced host innate immunity by binding to chitin oligosaccharides (Mentlak et al., 2012). Furthermore, effectors have been shown to target the microRNA biosynthesis pathway in plants (Qiao et al., 2015). Although the identification of these novel effectors and their target genes may shed light into the understanding of the blast mechanism, the question of how exactly these effectors suppress or evade host innate immunity, resulting in infection, still represents a challenge in the field of M. oryzae pathology.

Conclusions

The M. grisea species complex possesses a very broad host range, exhibits genetic variability and shows the emergence of new strains. Therefore, the exact naming of the rice blast fungus will be a long‐term effort with many questions needing to be discussed. Nevertheless, gaining a knowledge of the biology and genetic diversity of the M. grisea species complex is critical for an understanding of the blast mechanism and for the development of novel and sustained strategies to control rice blast and related fungal diseases.