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Nitrogen (N) deficiency is one of the critical environmental factors that induce leaf senescence, and its occurrence may cause the shorten leaf photosynthetic period and markedly lowered grain yield. However, the physiological metabolism underlying N deficiency-induced leaf senescence and its relationship with the abscisic acid (ABA) concentration and reactive oxygen species (ROS) burst in leaf tissues are not well understood. In this paper, the effect of N supply on several senescence-related physiological parameters and its relation to the temporal patterns of ABA concentration and ROS accumulation during leaf senescence were investigated using the premature senescence of flag leaf mutant rice (psf) and its wild type under three N treatments. The results showed that N deficiency hastened the initiation and progression of leaf senescence, and this occurrence was closely associated with the upregulated expression of 9-cis-epoxycarotenoiddioxygenase genes (NCEDs) and with the downregulated expression of two ABA 8′-hydroxylase isoform genes (ABA8ox2 and ABA8ox3) under LN treatment. Contrarily, HN supply delayed the initiation and progression of leaf senescence, concurrently with the suppressed ABA biosynthesis and relatively lower level of ABA concentration in leaf tissues. Exogenous ABA incubation enhanced ROS generation and MDA accumulation in a dose-dependent manner, but it decreased the activities of glutamine synthetase (GS) and glutamate dehydrogenase (GDH) in detached leaf. These results suggested that the participation of ABA in the regulation of ROS generation and N assimilating/remobilizing metabolism in rice leaves was strongly responsible for induction of leaf senescence by N deficiency.

The breeding of low phytic acid (lpa) crop is considered as an effective strategy to improve crop nutrition, but these crops have an inferior performance in seed germination. In this paper, two rice genotypes, cv. 9311 and its lpa mutant (9311-lpa), were used to clarify the relationship of InsP3 and ROS concentration in sprouting seeds with the occurrence of retarded seed germination for lpa crop. Results showed that the inferior performance of seed germination for 9311-lpa was mostly characterized by the delay of seed germination progression, with insignificant difference in seed germination rate between the two genotypes after a longer imbibition duration. The retarded seed germination of 9311-lpa was closely associated with the genotypic difference in InsP3 and ROS concentrations in germinating seeds, with the considerably higher InsP3 level and lower ROS concentration for 9311-lpa relative to the wild type. Under an appropriate range of concentration, exogenous H2O2 treatment promoted seed germination, while the activator of InsP3 (m-3M3FBS) had an inhibitory effect on seed germination. The delay of seed germination occurred mainly as the results of the higher InsP3 level and the lower ROS concentration in the germinating seeds of 9311-lpa. Furthermore, the germinating seeds of 9311-lpa had relatively lower activities of ROS scavenging enzymes (SOD, CAT, POD, and APX) and ROS generating enzyme (NOX) than those of the wild type. m-3M3FBS significantly suppressed NOX activity and NOX transcripts in sprouting seeds, which then resulted in the lowered ROS generation in sprouting seeds and the decreased seed germination rate. Thus, the retarded seed germination of 9311-lpa, with lower ROS level in germinating seeds, was mostly caused by the weaker ability of ROS generation in the presence of higher InsP3 level, rather than the effective detoxification of ROS burst during seed germination.

Abiotic stresses trigger premature leaf senescence by affecting some endogenous factors, which is an important limitation for plant growth and grain yield. Among these endogenous factors that regulate leaf senescence, abscisic acid (ABA) works as a link between the oxidase damage of cellular structure and signal molecules responding to abiotic stress during leaf senescence. Considering the importance of ABA, we collect the latest findings related to ABA biosynthesis, ABA signaling, and its inhibitory effect on chloroplast structure destruction, chlorophyll (Chl) degradation, and photosynthesis reduction. Post-translational changes in leaf senescence end with the exhaustion of nutrients, yellowing of leaves, and death of senescent tissues. In this article, we review the literature on the ABA-inducing leaf senescence mechanism in rice and Arabidopsis starting from ABA synthesis, transport, signaling receptors, and catabolism. We also predict the future outcomes of investigations related to other plants. Before changes in translation occur, ABA signaling that mediates the expression of NYC, bZIP, and WRKY transcription factors (TFs) has been investigated to explain the inducing effect on senescence-associated genes. Various factors related to calcium signaling, reactive oxygen species (ROS) production, and protein degradation are elaborated, and research gaps and potential prospects are presented. Examples of gene mutation conferring the delay or induction of leaf senescence are also described, and they may be helpful in understanding the inhibitory effect of abiotic stresses and effective measures to tolerate, minimize, or resist their inducing effect on leaf senescence.

Effect of high temperature (HT) on anthocyanin (ANS) accumulation and its relationship with reactive oxygen species (ROS) generation in color rice kernel was investigated by using a black kernel mutant (9311bk) and its wildtype (WT). 9311bk showed strikingly higher ANS content in the kernel than WT. Just like the starch accumulation in rice kernels, ANS accumulation in the 9311bk kernel increased progressively along with kernel development, with the highest level of ANS at kernel maturity. HT exposure evidently decreased ANS accumulation in 9311bk kernel, but it increased ROS and MDA concentrations. The extent of HT-induced decline in kernel starch accumulation was genotype-dependent, which was much larger for WT than 9311bk. Under HT exposure, 9311bk had a relatively lower increase in ROS and MDA contents than its WT. This occurrence was just opposite to the genotype-dependent alteration in the activities of antioxidant enzymes (SOD, CAT and APX) in response to HT exposure, suggesting more efficiently ROS detoxification and relatively stronger heat tolerance for 9311bk than its WT. Hence, the extent of HT-induced declines in grain weight and kernel starch content was much smaller for 9311bk relative to its WT. HT exposure suppressed the transcripts of OsCHS, OsF3&rsquo, H, OsDFR and OsANS and impaired the ANS biosynthesis in rice kernel, which was strongly responsible for HT-induced decline in the accumulation of ANS, C3G, and P3G in 9311bk kernels. These results could provide valuable information to cope with global warming and achieving high quality for color rice production.