Nitric oxide(NO)is a short-lived gaseous free radical that predominantly functions as a messenger and effector molecule.It affects a variety of physiological processes,including programmed cell death(PCD)through cyclic guanosine monophosphate(cGMP)-dependent and-independent pathways.In this field,dominant discoveries are the diverse apoptosis networks in mammalian cells,which involve signals primarily via death receptors(extrinsic pathway)or the mitochondria(intrinsic pathway)that recruit caspases as effector molecules.In plants,PCD shares some similarities with animal cells,but NO is involved in PCD induction via interacting with pathways of phytohormones.NO has both promoting and suppressing effects on cell death,depending on a variety of factors,such as cell type,cellular redox status,and the flux and dose of local NO.In this article,we focus on how NO regulates the apoptotic signal cascade through protein S-nitrosylation and review the recent progress on mechanisms of PCD in both mammalian and plant cells.
Combined approaches with genetics, biochemistry, and proteomics studies have greatly advanced our understanding of brassinosteroid （BR） signaling in Arabidopsis. However, in rice, a model plant of monocot and as well an important crop plant, BR signaling is not as well characterized as in Arabidopsis. Recent studies by forward and reverse genetics have identified a number of either conserved or specific components of rice BR signaling pathway, bringing new ideas into BR signaling regulation mechanisms. Genetic manipulation of BR level or BR sensitivity to improve rice yield has established the great significance of BR research achievements.
