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Root meristem activity determines root growth and root architecture and consequently affects water and nutrient uptake in plants. However, our knowledge about the regulation of root meristem activity in crop plants is very limited. Here, we report the isolation and characterization of a short root mutant in rice () with reduced root meristem activity. This root growth defect is caused by a mutation in (), which encodes a 3-hydroxyacyl-CoA dehydrogenase, an enzyme involved in β-oxidation. The reduced root meristem activity of results from reduced salicylic acid (SA) levels and can be rescued by SA application. Furthermore, reduced SA levels are associated with reduced levels of reactive oxygen species (ROS) in, likely due to increased expression of redox and ROS-scavenging-related genes, whose increased expression is (at least in part) caused by reduced expression of the SA-inducible transcriptional repressors WRKY62 and WRKY76. Like SA, ROS application substantially increased root length and root meristem activity in These results suggest that AIM1 is required for root growth in rice due to its critical role in SA biosynthesis: SA maintains root meristem activity through promoting ROS accumulation by inducing the activity of WRKY transcriptional repressors, which repress the expression of redox and ROS-scavenging genes.

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Eight rice varieties with wide diversity in apparent amylose content (AC) were selected and planted in the early season and late season of Hangzhou and in the winter season of Hainan for two consecutive years to study the genotype x environment effects on the starch properties of the grain. Analyses of variance showed that AC, cool paste viscosity, breakdown viscosity, setback viscosity, peak time, gel hardness, adhesiveness, and cohesiveness were mainly affected by genotypic variation, whereas peak viscosity and hot paste viscosity were mainly affected by environmental variation. The year x season, year x variety, seasonx variety, and year x season x variety effects were significant for most traits, indicating significant genotype x environment interactions. AC was significantly correlated with all other parameters except PV. Because the Wx gene controls the synthesis of amylose in rice, the mechanism of how the environment affects starch properties is discussed in relation to Wx expression and regulation. The implications of the results for rice breeders and starch-based food manufacturers are discussed.

BackgroundHypoxia/reoxygenation(H/R)-induced apoptosis of cardiomyocytes plays an important role in myocardial injury. Lycopene is a potent antioxidant carotenoid that has been shown to have protective properties on cardiovascular system. The aim of the present study is to investigate the potential for lycopene to protect the cardiomyocytes exposed to H/R. Moreover, the effect on mitochondrial function upon lycopene exposure was assessed.Methods and FindingsPrimary cardiomyocytes were isolated from neonatal mouse and established an in vitro model of H/R which resembles ischemia/reperfusion in vivo. The pretreatment of cardiomyocytes with 5 µM lycopene significantly reduced the extent of apoptosis detected by TUNEL assays. To further study the mechanism underlying the benefits of lycopene, interactions between lycopene and the process of mitochondria-mediated apoptosis were examined. Lycopene pretreatment of cardiomyocytes suppressed the activation of the mitochondrial permeability transition pore (mPTP) by reducing the intracellular reactive oxygen species (ROS) levels and inhibiting the increase of malondialdehyde (MDA) levels caused by H/R. Moreover, the loss of mitochondrial membrane potential, a decline in cellular ATP levels, a reduction in the amount of cytochrome c translocated to the cytoplasm and caspase-3 activation were observed in lycopene-treated cultures.ConclusionThe present results suggested that lycopene possesses great pharmacological potential in protecting against H/R-induced apoptosis. Importantly, the protective effects of lycopene may be attributed to its roles in improving mitochondrial function in H/R-treated cardiomyocytes.

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