Proteome analysis and characterization of phenotypes of lesion mimic mutantspotted leaf 6in rice

Abstract

Rice spotted leaf 6 (spl6) mutant produces lesions caused by spontaneous cell death in the absence of pathogenic infection. Expression of this genetic trait was developmentally programmed. After the tillering stage, small red and brown lesions were initiated in groups on the leaf blade. Eventually, the lesions formed parallel lines along the midrib of the leaf. Under light and transmission electron microscopy, we observed that thylakoid membranes of mesophyll chloroplasts were progressively damaged in the nonspotted section of the mutant leaf. However, chloroplasts were absent in the mesophyll cells of the spotted area of the spl6 mutant. These results indicated that lesion formation of the spl6 mutant might be caused by oxidative burst. Proteome analysis revealed that 159 protein spots were up or downregulated in comparison between spotted leaves of the spl6 mutant plants and normal leaves of the wild type. Among them, protein disulfide isomerase (PDI), transketolase, thioredoxin peroxidase (TPX), ATP synthase, RuBisCO large subunit, and RuBisCO activase small subunit were not identified in the spl6 mutant but were abundant in the wild type. Especially, the absence of TPX and PDI might be the cause of the failure to protect cells against oxidative burst resulting in degradation of the thylakoid membranes and leading to programmed cell death and lesion development.

Proteomic characterization of the Rph15 barley resistance gene-mediated defence responses to leaf rust

“…In Bowman- Rph15 inoculated sample was in fact evaluated a reduction of 38.2%, 84.1%, 75.28% and 10.12% of the RuLC degraded forms with respect to the control sample respectively for the major bands of the degradation forms numbered from 1 to 5 (Figure 4B). A similar RuLC degradation trend was observed in rice as induced by bacterial blight infection, in lesion mimic mutants [24-26] and in wheat after Fusarium graminearum infection [19]. Taken together, our results support the conclusion that in the resistant genotype Bowman- Rph15 the Rubisco integrity was more preserved after infection with respect to control sample.…”

Proteomic analysis of a disease-resistance-enhanced lesion mimic mutant spotted leaf 5 in rice

“…According to our 2-DE data and the proteomic results of other rice lmms (Takahashi et al 2003; Tsunezuka et al 2005; Jung et al 2006; Kang et al 2007; Kim et al 2008), proteins involved in ROS scavenging, defense responses or cell death such as SOD ( spl1 , blm ), CAT ( spl6 , blm ), Peroxidase ( spl1 ), APX ( spl5 , blm ), GST ( cdr2 , spl5 ), were likely to be induced in lmms , whereas proteins involved in photosynthesis and glycolysis such as Rubisco ( spl1 , spl5 , spl6 , blm , crd2 ), Rubisco-A ( spl5 , spl6 ), and GAPDH ( spl1 , spl5 , cdr2 ) were often deceased in lmms ; defense-related protein like OsPR5 ( spl1 ), OsPR10 ( blm ), PBZ1 ( spl1 , cdr2 , blm ), Chia2a ( spl5 ) were significantly activated in lmms . This suggests that the differential accumulation of these proteins is common features for lmms .…”

“…Moreover, in the present study we found that Rubisco activases (Rubisco-A), which catalyze Rubisco activation, were also down-regulated in spl5 mutant (Table 1). The reduction of Rubisco and/or Rubisco-A was also found in the lmms of spl1 (Kim et al 2008), spl6 (Kang et al 2007), crd2 (Tsunezuka et al 2005), and blm (Jung et al 2006), suggesting that the reduction in Rubisco and Rubisco-A accumulation is a shared phenomenon among lmms .…”

“…The comparative proteomics has been used to identify differentially expressed proteins between wild type (WT) rice and lmms (Takahashi et al 2003; Tsunezuka et al 2005; Jung et al 2006; Kang et al 2007; Kim et al 2008). However, different defense-related proteins and metabolic enzymes were found to be differently accumulated during lesion formation in a lmm -specific manner or in different lmms .…”

Mutagenic effects of heavy ion irradiation on rice seeds

“…After gene mapping, the spl30 locus was found to be located on the long arm of chromosome 9, a location that was not previously reported for the spl gene. The spl33 locus was found to be located on the long arm of chromosome 1, which differs from that of the other two loci (spl6 and spl28) [29,30]. We therefore might have uncovered new genes involved in lesion mimic that provide valuable materials for the study of mechanisms underlying leaf death and disease resistance.…”