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Stigma exsertion rate (SER) of the male sterile line is a key limiting factor for hybrid seed production in rice. Although a large number of quantitative trait loci associated with SER have been reported, few genes have been molecularly cloned and functionally characterized, severely hindering the genetic improvement of SER of the male sterile line and the breeding efficiency of hybrid rice. In this study, we identified three grain shape regulatory genes, GS3, GW8 and GS9, as potential candidate genes for targeted manipulation of grain shape and SER. We show that simultaneously knocking out these three genes could effectively increase SER by increasing the ratio of spikelet length/spikelet width and length of stigma and style, without negative impacts on other agronomic traits. Cellular examination and transcriptomic analyses revealed a role of these genes in coordinated regulation of transverse and longitudinal cell division in the pistils. Moreover, we demonstrate that targeted manipulation of these grain shape genes could significantly improve the outcrossing rate in both the ZH11 (a japonica variety) and Zhu6S (an indica male sterile line) backgrounds. Our results provide new insights into the mechanisms of rice SER regulation and develop an effective strategy to improve SER and out-crossing rate in rice, thus facilitating hybrid rice production.

The Ala–Val–Thr–Phe (AVTF) peptide derived from edible Dendrobium aphyllum was co-incubated with Lactobacillus amylolyticus in a previous study. The aim of the present study was to further examine the antioxidative and protective effects of the AVTF peptides through the analysis of free-radical quenching in HepG2 cells subjected to 2,2-azobis(2-methylpropanimidamidine)dihydrochloride (AAPH)-induced oxidative stress and to determine the active sites within the peptide. Variations in intracellular malondialdehyde levels indicated that these peptides protect HepG2 cells by preventing ROS attack and lipid peroxidation. Antioxidant enzymes and Nrf2 were downregulated in AVTF-treated but not in AAPH-treated HepG2 cells, whereas the electrically sensitive Keap1 was not susceptible to free radical-induced damage after AVTF treatment. However, this did not result in the activation of the Nrf2/Keap1 signaling pathway, thus indicating that one potential mechanism by which AVTF maintains homeostasis in HepG2 cells is by directly scavenging free radicals. Furthermore, quantum chemical calculations and the assessment of electronic-related properties associated with antioxidant activity revealed that the active sites of AVTF included N9–H11, which was further confirmed by the assessment of ROS levels in methylated AVTF-treated cells. The results of this study provide valuable insights into the active site N9–H11 in the Ala residue of AVTF, which influences the antioxidant activity of the peptide.

We simulated 2 types of external injuries in fruitlets—throwing and cutting with knife, and evaluated the degree of putrefaction. The external injury-induced toxicity was determined by observing changes in the spatial structure of the cells. Next, we determined the contents of lignin and total flavonoids, and the expression of phenylpropanoid pathway-related genes encoding enzymes that alleviate peroxidation toxicity. By measuring the content of naringin, we uncovered a non-enzymatic antioxidant mechanism that eliminates excessive reactive oxygen species (ROS) in fruitlets. We also determined that external injury triggers an increased activity of antioxidant enzymes. Overall, in fruitlets, external injuries activate naringin biosynthesis in response to stress.