**5. Resistance of rice**

### **5.1 Sources and inheritance of RFS resistance**

Various attempts have been made to screen rice cultivars resistant to RFS. Screening of 186 rice hybrids to RFS resistance was done by Liang and

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*Rice False Smut: An Increasing Threat to Grain Yield and Quality*

with Pujiang 6 to construct gene mapping populations [67].

responsible for RFS resistance are still unknown.

**5.2 Molecular basis of RFS resistance**

colleagues [64], which identified few hybrids with low disease incidence. They screened the commercial hybrids that had lower rates of diseased panicles and infected florets at Xindu and Qionglai (Sichuan Province, China) in 2011 together with newly registered varieties. Lore et al. [65] evaluated some hybrids and inbred cultivars growing across India for susceptibility/tolerance to RFS. Artificial inoculation of false smut was done by Kaur et al. [66], which identified nine hybrids resistant to RFS among 125 rice genotypes screened. More detailed evaluation of RFS resistance was performed by Huang and colleagues [67]. A total of 843 rice accessions were screened in disease nurseries in 3 years although some of those accessions were planted in different locations and on different dates. Finally, 36 accessions were found to show no disease incidence. A highly susceptible accession Pujiang 6 was identified in this study. Polymorphism analysis determined several resistant accessions which could be used for crossing

Resistance of genes against *V. virens* has not been identified yet, but numerous efforts have been undertaken to study the inheritance of the resistance. Earlier, using 266 near-isogenic introgression lines derived from susceptible cultivar Teqing and resistant Lemont and natural infection data in the field, Xu et al. [68] identified two RFS resistance-contributing QTLs, *QFsr10* and *QFsr12*, located on chromosome 10 and 12, respectively. Later, the same group further identified 10 QTLs for RFS resistance [69]. Li et al. [70] developed a population of 157 recombinant inbred lines (RILs) from crossing a susceptible landrace Daguandao (*O. sativa* subsp. japonica) and a resistant cultivar IR28 (*Oryza sativa* subsp. indica). Subsequently, different RILs and parents were evaluated following effective artificial inoculation under field conditions. Genetic analysis showed that the RFS resistance was controlled by two major genes with equal effect of 11.41 and polygenes with minor effects. Further work identified seven QTLs for RFS resistance on chromosomes 1, 2, 4, 8, 10, 11, and 12, and the phenotypic variance ranged from 9.8 to 22.5% [71]. The inheritance of RFS resistance in two-line hybrid rice was investigated using natural infection technique. When a moderate susceptible sterile line TGMS 33S was crossed with susceptible restorer lines, the F1 was susceptible to RFS; when TGMS 33S was crossed with resistant restorer lines, 87% of the F1 showed dominant or incomplete dominant inheritance of RFS resistance, the rest showed recessive inheritance [72]. It should be noted that natural infection of RFS varies among fields and seasons, efficient artificial inoculation method is highly recommended to validate the disease phenotype. Although some progresses on screening for resistant materials and determining the resistance inheritance have been achieved, genes

Since many rice cultivars with high RFS resistance or high susceptibility have been identified, comparative transcriptome analysis is a promising method to mine resistance- or susceptibility-related genes in rice. For instance, time-course RNAseq was carried out on susceptible cultivar LYP9 and resistant cultivar IR28 upon *V. virens* infection [62]. Data analysis revealed that many defense-related genes were only up-regulated in the resistant cultivar IR28, but not in LYP9. Particularly, phytoalexin biosynthetic pathway genes such as *OsCPS2*, *OsMAS*, and *OsKSL11* were significantly induced in IR28 at early infection stages, indicating that phytoalexins may contribute to rice resistance against RFS. *PR* family genes, such as β-1,3 glucanase and chitinase genes, were specifically up-regulated in IR28, while generally down-regulated in LYP9. Moreover, a chitinase gene cluster was found close to a RFS resistance QTL on chromosome 11 [71], and nine genes in this cluster were

*DOI: http://dx.doi.org/10.5772/intechopen.84862*

*Protecting Rice Grains in the Post-Genomic Era*

ized to function in the flower infection of *V. virens*.

**4.4 Host compatible interaction with** *V. virens*

susceptible rice cultivars infected with *V. virens* [42, 62]*.*

the contrary, some effectors of *V. virens* could induce cell death or defense response in rice protoplast. For example, UV\_44 induces cell death, and this ability relies on the serine peptidase active sites. UV\_1423 could be *N*-glycosylated, which affects its ability to trigger cell death [56]. However, so far, no effectors have been character-

Nevertheless, several virulence factors have been identified in *V. virens*. UvSUN2 is a SUN domain protein; loss of function of this factor results in inability of infecting rice flower, as well as abnormal stress responses and mycelium growth [57]. Mutation in *UvPRO1* increases sensitivity to abiotic stresses and attenuates virulence, in addition to impaired growth rate and sporulation [49]. In contrast, a low-affinity iron transporter encoded by *Uvt3277* negatively regulates virulence in *V. virens* [58].

Monitoring host responses to *V. virens* infection could help to uncover the pathogenesis of RFS. In an earlier transcriptome study, a series of differentially expressed genes have been identified in a susceptible rice cultivar 93-11 infected with a field *V. virens* isolate [59]. Among them, genes regulated by Ca2+ or abscisic acid are down-regulated, while genes regulated by Myb or WRKY transcription factors are up-regulated. *OsSWEET11* and *OsSWEET14*, which may be involved in disease susceptibility [60], are also up-regulated by *V. virens* infection. Specifically, many pollen development associated genes are down-regulated by *V. virens* infection, but not responsive to other biotic and abiotic stresses, suggesting that these genes may play unique roles in rice-*V. virens* interaction [59]. Additionally, several transcriptome analyses on compatible rice-*V. virens* interactions have been reported. Genes involved in hydrolase, transporter, and flower development tend to be downregulated in susceptible cultivar Huang-Xiu-Zan upon infection [61]. Expression of many defense-related genes such as *PAL* and *PR* genes could be suppressed in

As a successful pathogen, *V. virens* should have abilities to set up colonization in rice floral organs and acquire abundant nutrients for propagation, in addition to subvert rice immunity. Transcriptome analysis reveals that genes associated with flower opening, such as *ARF6* and *ARF8* homologs, are down-regulated by *V. virens* infection [42]. This may contribute to inhibition of flower opening during RFS pathogenesis [42]. Furthermore, *V. virens* infection causes failure of ovary fertilization. However, a number of grain-filling-specific genes, such as seed-specific starch synthesis related genes and those encoding seed storage proteins, are activated for high expression in *V. virens*-infected rice spikelets [42]. It is suggested that *V. virens* may be able to mimic fertilization and hijack rice grain-filling system for nutrient supply to pathogen growth and RFS ball formation. This finding is further supported by an independent study [63]. Although the underlying mechanism needs further investigation, the observation of *V. virens* activating rice grain filling could provide a promising explanation why mild *V. virens* infection enhances rice yield traits, including grain weight and filled grain number [9]. Identification and characterization of *V. virens* factors that manipulate rice grain filling should be an interesting research area in the future.

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**5. Resistance of rice**

**5.1 Sources and inheritance of RFS resistance**

Various attempts have been made to screen rice cultivars resistant to RFS. Screening of 186 rice hybrids to RFS resistance was done by Liang and colleagues [64], which identified few hybrids with low disease incidence. They screened the commercial hybrids that had lower rates of diseased panicles and infected florets at Xindu and Qionglai (Sichuan Province, China) in 2011 together with newly registered varieties. Lore et al. [65] evaluated some hybrids and inbred cultivars growing across India for susceptibility/tolerance to RFS. Artificial inoculation of false smut was done by Kaur et al. [66], which identified nine hybrids resistant to RFS among 125 rice genotypes screened. More detailed evaluation of RFS resistance was performed by Huang and colleagues [67]. A total of 843 rice accessions were screened in disease nurseries in 3 years although some of those accessions were planted in different locations and on different dates. Finally, 36 accessions were found to show no disease incidence. A highly susceptible accession Pujiang 6 was identified in this study. Polymorphism analysis determined several resistant accessions which could be used for crossing with Pujiang 6 to construct gene mapping populations [67].

Resistance of genes against *V. virens* has not been identified yet, but numerous efforts have been undertaken to study the inheritance of the resistance. Earlier, using 266 near-isogenic introgression lines derived from susceptible cultivar Teqing and resistant Lemont and natural infection data in the field, Xu et al. [68] identified two RFS resistance-contributing QTLs, *QFsr10* and *QFsr12*, located on chromosome 10 and 12, respectively. Later, the same group further identified 10 QTLs for RFS resistance [69]. Li et al. [70] developed a population of 157 recombinant inbred lines (RILs) from crossing a susceptible landrace Daguandao (*O. sativa* subsp. japonica) and a resistant cultivar IR28 (*Oryza sativa* subsp. indica). Subsequently, different RILs and parents were evaluated following effective artificial inoculation under field conditions. Genetic analysis showed that the RFS resistance was controlled by two major genes with equal effect of 11.41 and polygenes with minor effects. Further work identified seven QTLs for RFS resistance on chromosomes 1, 2, 4, 8, 10, 11, and 12, and the phenotypic variance ranged from 9.8 to 22.5% [71]. The inheritance of RFS resistance in two-line hybrid rice was investigated using natural infection technique. When a moderate susceptible sterile line TGMS 33S was crossed with susceptible restorer lines, the F1 was susceptible to RFS; when TGMS 33S was crossed with resistant restorer lines, 87% of the F1 showed dominant or incomplete dominant inheritance of RFS resistance, the rest showed recessive inheritance [72]. It should be noted that natural infection of RFS varies among fields and seasons, efficient artificial inoculation method is highly recommended to validate the disease phenotype. Although some progresses on screening for resistant materials and determining the resistance inheritance have been achieved, genes responsible for RFS resistance are still unknown.
