A novel lesion mimic gene and mapping
Lesion mimic is disease-like phenomenon appears to plant leaves without any pathogens infection, injury and obvious stress . The phenotype of LM in the current study is like some yellow spots lesions on wheat leaves, and lesion spots booting in the fifth or sixth leaf stage in wheat. The previously reported LM gene in wheat such as lm was located on the 1BL , lm1 and lm2 were located on 3BS and 4AL , lm3 was mapped on 3BL . Unlike the previously reported lesion mimic genes, the LM gene (lm4) found in this study was a novel type of lesion-mimic gene in wheat, which mapped on 2DS and it’s a dominant LM gene derived from Yanzhan1/Neixiang188 RILs. It (lm4) also does not like HLP mutant induced by EMS . Although LM traits are almost at fifth or sixth leaf stage expression, LM was a naturally mutated phenotype, and the type of lesion manifestation also different in this study. The LM phenotype induced by EMS is small white color spots (1~2mm) on the leaves . Therefore, the LM found is different from the EMS-induced mutant, which is a novel type of lesion mimic (lm4) that different from previously reported LM genes.
The relationship between LM and yield traits in wheat
Previous research found that most lesion mimics have a negative effect on crops agronomic traits, especially affecting the yield production, but not include HLP mutant [12, 16, 26]. In the current study, the agronomic traits including yield traits (SPI, SSNS, GNS and TGW) in wheat RILs has not significant reduced by appearance of lesion mimic phenotype comparing with normal wheat lines (Table 2). The purpose of the breeders is to breed disease-resistant and high yield-producing crop varieties. The lm4 located in this study significantly improved the resistance to stripe rust in wheat and would not affect major yield related traits, which can be a potential tool for future disease resistance breeding.
The effects of lesion mimics on stripe rust resistance
Stripe rust is a major fungal disease that threatens the quality and yield of wheat . Controlling the spread of stripe rust and breeding new resistant varieties to improve the quality and yield of wheat is the main purpose of breeders. In addition, except for discover disease resistance genes for specially races, study on some related disease resistance genes has gradually attracted attention in recent years. Li et al. reported lm (derived from Ning7840 located on 1BL) can enhance leaf rust resistance in wheat . lm1 and lm2 mapped on 3BS and 4AL were correlation with improving powdery mildew. Recently located LM gene lm3 (mapped on 3BL) has adult-plant resistance to powdery mildew . These results provide new insight into the molecular mechanism of LM and broad-spectrum resistance in wheat，which may be helpful for screening candidate genes underlying LM trait in wheat. In this study, lm4 is a novel lesion-mimic gene that related to enhancing stripe rust resistance in wheat. There are certain reported QTLs for stripe rust, fusarium head blight resistance and leaf rust on 2DS in wheat closed to lm4 [28-33]. In this study, a significant correlation found between LM and stripe rust resistant in the field (r=-0.61, p<0.01). The potential of lm4 on the above diseases in wheat deserve to be further studied.
The related signal pathways of lesion mimic
In recent years, studies have reported that the lesion mimics resembling a hypersensitivity reaction may enhance the resistance of plants by certain defense signal pathways, which involved in plant disease resistance or stress resistance. Some LM associated with ROI production, which response to cell death signal [3, 34, 35]. The inducible defense response of plants is mainly to provide plants with an optimal defense system by relying on signaling pathways such as salicylic acid, jasmonic acid and ethylene, and the cross-action between them. And salicylic acid-dependent pathway leading to cell death. In plants, cell death may play an important role in resistance to pathogens .
In addition, studies have reported that LM may be associated with a programmed cell death signaling pathway, because pathogens are difficult to invade the necrotic spots, thereby improving plant disease resistance . Plants have complex systems for regulating cell death and these systems have a purpose in development of the plant against pathogens and environmental stress . These results indicate that the mechanism of LM regulation or enhancement of plant resistance may cause linkage with resistance genes or involved in the signal pathway to regulate plant defense responses, regulating the pathway of programmed cell death in plant. In this study, we determined lm4 in to a 50 Mb interval on 2DS, and 18 predicted candidate genes in it (Table S1). Among of these candidate genes, TraesCS2D02G090600 was related to physiological defense response and immunity protein activity; and TraesCS2D02G091200, TraesCS2D02G092200 are involved in regulate cell death and defense when the pathogen is recognized; TraesCS2D02G090900 and TraesCS2D02G091100 are relate to signal transduction. The function of TraesCS2D02G091000, TraesCS2D02G091600, TraesCS2D02G091900 and TraesCS2D02G092100 are response to stimulus. TraesCS2D02G091300 and TraesCS2D02G091400 are related to leaf senescence and chloroplast, respectively.
Lesion mimic mutants could be a powerful tool to study their involvement in cell death. Besides this genetic approach, physiological and biochemical characterization of the proteins corresponding to identified the function of LM genes. It should be provide insight into in cell death, defense or development, through the determination of their biochemical function, subcellular localization and the interacting proteins . In the present study, fine mapping or gene cloning are required to understand the resistance mechanism and function of lm4. Studying the LM gene and function is crucial for understanding the signaling pathways of plant apoptosis and disease resistance mechanism. Cloning the gene responsible for lm4 will help us to further understand the complex plant disease resistance network.