A 3-bp deletion of WLS5 gene leads to weak growth and early leaf senescence in rice

Abstract

Background: In rice (Oryza sativa) and other grains, weak growth (dwarfism, short panicle length, and low seedsetting rate) and early senescence lead to reduced yield. The molecular mechanisms behind these processes have been widely studied; however, the complex genetic regulatory networks controlling growth and senescence require further elucidation. Results: We isolated a mutant exhibiting weak growth throughout development and early senescence of leaf tips, and designated this mutant weakness and leaf senescence5 (wls5). Histological analysis showed that the poor growth of wls5 plants involved a reduction in cell length and number. Physiological analysis and transmission electron microscopy revealed that the wls5 cells had abnormal chloroplasts, and the mutants underwent chlorophyll degradation triggered by accumulation of reactive oxygen species. Consistent with this, RNA sequencing revealed changes in senescencerelated gene expression in wls5 plants. The wls5 mutants also exhibited significantly higher stomatal density and altered phytohormone contents compared with wild-type plants. Fine mapping delimited WLS5 to a 29-kb region on chromosome 5. DNA sequencing of wls5 identified a 3-bp deletion in the first exon of LOC_Os05g04900, resulting in a deletion of a lysine in the predicted protein. Knockout of LOC_Os05g04900 in Nipponbare plants caused leaf senescence, confirming this locus as the causal gene for WLS5. Conclusions: We identified a novel mutant (wls5) that affects plant development and leaf senescence in rice. LOC_Os05g04900, encoding a protein of unknown function, is the causal gene for wls5. Further molecular study of WLS5 will uncover the roles of this gene in plant growth and leaf senescence.

Rice EARLY SENESCENCE 2, encoding an inositol polyphosphate kinase, is involved in leaf senescence

“…2 h, j-l). This is consistent with previous reports concerning early senescence mutants in rice [ 17 , 73 , 89 – 91 ]. Therefore, it is indicates that the increased SOD activity in es2 was due to high O 2 − production and reducedCAT activity accelerated accumulation of H 2 O 2 .…”

Identification and genetic analysis of EMS-mutagenized wheat mutants conferring lesion-mimic premature aging

“…It was found [44] that water deficit during grain filling period could cause premature senescence of flag leaves, but the senescence process could be delayed by changing hormone concentration of plants. There are many reasons for rice premature aging, for example, the effect of NAC transcription factors on abscisic acid (ABA) [25], the functional impairment of calcium-dependent protein kinase OsCPK12 [28], the deletion of gene fragment [29], the response and regulation of genes related to antioxidant and carbohydrate metabolism [45], and so on. Based on the research experience of rice early senescence, further work should be focused on the cloning and functional verification of candidate gene for premature aging.…”

“…OsCPK12 [28]. The 3-bp deletion in the gene of WLS5 also leads to premature senescence in rice [29]. The early senescence mutations esl2 [30], esl3 [31], esl4 [32], esl5 [33], and esl6 [34] selected by the Rice Research Institute of Southwest University by EMS mutation were controlled by mononuclear genes.…”

Identification and genetic analysis of EMS-mutagenized wheat mutants conferring lesion-mimic premature aging

“…It was found [37] that water deficit during grain filling period could cause premature senescence of flag leaves, but the senescence process could be delayed by changing hormone concentration of plants. There are many reasons for rice premature aging, for example, the effect of NAC transcription factors on abscisic acid (ABA) [19], the functional impairment of calcium-dependent protein kinase OsCPK12 [22], the deletion of gene fragment [23], the response and regulation of genes related to antioxidant and carbohydrate metabolism [38], and so on. Based on the research experience of rice early senescence, further work should be focused on the cloning and functional verification of candidate gene for premature aging.…”

“…Signs of senescence began to appear in the rice premature senescence mutant es4 in about 60 days, due to the loss of function of the calcium-dependent protein kinase OsCPK12 [22]. The 3-bp deletion in the gene of WLS5 also leads to premature senescence in rice [23]. The early senescence mutations esl2 [24], esl3 [25], esl4 [26], esl5 [27], and esl6 [28] selected by the Rice Research Institute of Southwest University by EMS mutation were controlled by mononuclear genes.…”