Abstract
Lesion mimic mutants (LMMs) are usually controlled by single recessive mutations that cause the formation of necrotic lesions without pathogen invasion. These genetic defects are useful to reveal the regulatory mechanisms of defense-related programmed cell death in plants. Molecular evidence has been suggested that some of LMMs are closely associated with the regulation of leaf senescence in rice (Oryza sativa). Here, we characterized the mutation underlying spotted leaf4 (spl4), which results in lesion formation and also affects leaf senescence in rice. Map-based cloning revealed that the γ ray-induced spl4-1 mutant has a single base substitution in the splicing site of the SPL4 locus, resulting in a 13-bp deletion within the encoded microtubule-interacting-and-transport (MIT) spastin protein containing an AAA-type ATPase domain. The T-DNA insertion spl4-2 mutant exhibited spontaneous lesions similar to those of the spl4-1 mutant, confirming that SPL4 is responsible for the LMM phenotype. In addition, both spl4 mutants exhibited delayed leaf yellowing during dark-induced or natural senescence. Western blot analysis of spl4 mutant leaves suggested possible roles for SPL4 in the degradation of photosynthetic proteins. Punctate signals of SPL4-fused fluorescent proteins were detected in the cytoplasm, similar to the cellular localization of animal spastin. Based on these findings, we propose that SPL4 is a plant spastin that is involved in multiple aspects of leaf development, including senescence.
Highlights
Among the defense mechanisms activated in response to pathogen attacks in plants, the hypersensitive response (HR), which induces rapid death of infected cells, prevents the spread of pathogens to adjacent cells (Morel and Dangl, 1997; Takahashi et al, 2009)
When N8 and spl4-1 plants were grown in the paddy field (Suwon, South Korea, 37◦N latitude), autonomous lesions began to appear in the second leaves of the spl4-1 mutant at the maximum tillering stage (87 days after sowing, DAS) (Figures 1A,B), and expanded throughout the entire leaf at the heading stage (118 DAS), except for the flag leaves (Figures 1C,D)
We found that the greenness of spl4-1 leaves persisted much longer than that of N8 leaves around the grain harvest stage (162 DAS) (Figure 1E)
Summary
Among the defense mechanisms activated in response to pathogen attacks in plants, the hypersensitive response (HR), which induces rapid death of infected cells, prevents the spread of pathogens to adjacent cells (Morel and Dangl, 1997; Takahashi et al, 2009). A spotted leaf gene Spl encodes a heat shock protein and its mutation is responsible to lesion formation in the rice leaves (Yamanouchi et al, 2002). Mutation of SPL5 encoding a putative splicing factor 3b subunit 3 (SF3b3) continuously developed small reddish-brown necrotic lesions on the rice leaves (Chen et al, 2012). Impairment of COPROPORPHYRINOGEN III OXIDASE (CPOX) in the rice lesion initiation 1 (rlin1) mutant causes the formation of necrotic lesions in rice leaves and stems due to excessive ROS accumulation (Sun et al, 2011). SPL11 encodes a U-box/armadillo repeat protein conferring E3 ubiquitin ligase activity and the spl mutant displays a spontaneous cell death phenotype and enhanced resistance to fungal and bacterial diseases in rice (Zeng et al, 2004)
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