Reactive oxygen species and nitric oxide induce senescence of rudimentary leaves and the expression profiles of the related genes in Litchi chinensis

Abstract

Litchi is one of the most important subtropical evergreen fruit trees in southern Asia. Previous studies indicated that high-temperature conditions encourage growth of rudimentary leaves in panicles and suppress flowering. We have demonstrated that methyl viologen dichloride hydrate (MV) and sodium nitroprusside (SNP) promoted flowering in litchi partially by inhibiting the growth of rudimentary leaves via reactive oxygen species (ROS) and nitric oxide (NO). In the present study, we examined the microstructure and ultrastructure, programmed cell death (PCD) ratio, nuclei morphology of the rudimentary leaves, and the expression of senescence-related genes after the treatment with ROS or NO. The results showed that chromatins of the ROS- or NO-treated cells in the rudimentary leaves were condensed. Fusion of the cytoplasm-digesting vesicles with the vacuole and degradation of cytoplasm forming scattered debris were found in those of the treated cells. Treatment with ROS or NO increased the cell PCD ratio. Morphology of the nuclei stained by propidium iodide (PI) showed that nuclei shape became irregular after the ROS or NO treatment. Further, the expression levels of LcRboh, LcMC-1-like, and LcPirin were higher in the ROS- and NO-treated rudimentary leaves than those in the control ones, suggesting that these genes may be involved in the ROS and NO-induced senescence and abscission of the rudimentary leaves in litchi. Our results suggested that ROS and NO play an important role in inducing the senescence of the rudimentary leaves, and ROS- and NO-induced PCD may be involved in the regulation of the rudimentary leaf growth in litchi.

Transcriptome Analysis of Pistacia vera Inflorescence Buds in Bearing and Non-Bearing Shoots Reveals the Molecular Mechanism Causing Premature Flower Bud Abscission

“…PA catabolism by amine oxidases, copper-containing amine oxidases (CuAOs), flavin-containing PA oxidases (PAOs) and the parallel production of H 2 O 2 can result in two different scenarios. High H 2 O 2 levels lead to programmed cell death (PCD) [72], while low H 2 O 2 level is efficiently scavenged by enzymatic/nonenzymatic antioxidant factors that help plants to survive abiotic stress, using different defense mechanisms [73]. In the present study, ROS related genes such as peroxisome 1 (PEX1), isocitrate dehydrogenase, COPPER/ZINC SUPEROXIDE DISMUTASE, FLAVANONE 3-HYDROXYLASE, Peroxidase, HXXXD-type acyl-transferase family protein as well as many stress-related genes (Disease resistance protein, Glycosyl hydrolase, Cysteine-rich secretory proteins, Serine/threonine-protein kinase MAPK/ERK KINASE 4, VASCULAR ASSOCIATED DEATH1, Leucine-rich repeat protein kinase, Riboflavin synthase-like superfamily protein and Pentatricopeptide repeat) were found down-regulated in June "OFF" inflorescence buds vs June "ON" inflorescence buds.…”

Assessment of Subcellular ROS and NO Metabolism in Higher Plants: Multifunctional Signaling Molecules

“…Yang et al [183] have elucidated senescence-inducing ROS-NO crosstalk in litchi plants and have described the morphological, structural, PCD, and expression characteristics of senescence genes after treatment with ROS and NO. Their results show the distorted structure and morphology as well as the upregulation of LcRBOH, LcMC-1-like and LcPirin genes, which play a role in ROS-and NO-mediated senescence and leaf abscission in litchi plants [183]. NO and ROS have also been reported to play a vital role in signaling cascades and defense mechanisms in legumes and rhizobia [184].…”

Genome-wide transcriptome analysis reveals the molecular mechanism of high temperature-induced floral abortion in Litchi chinensis

“…We have previously focused on the feature of the low temperature-, ROS-, and NO-induced senescence of panicle leaves, and found that programmed cell death (PCD) is involved in the panicle leaf growth regulation by ROS and NO, as well as by low temperature in litchi [6, 8]. We also screened PCD related genes from our RNA-seq data sets of the ROS-treated rudimentary leaves [9], and identified a litchi homolog MCII ( LcMCII-1 ).…”