Organisms have evolved endogenous biological clocks as internal timekeepers to coordinate metabolic processes with the external environment. Here, we seek to understand the mechanism of synchrony between the oscillator and products of metabolism known as Reactive Oxygen Species (ROS) in Arabidopsis thaliana . ROS-responsive genes exhibit a time-of-day–specific phase of expression under diurnal and circadian conditions, implying a role of the circadian clock in transcriptional regulation of these genes. Hydrogen peroxide production and scavenging also display time-of-day phases. Mutations in the core-clock regulator, CIRCADIAN CLOCK ASSOCIATED 1 ( CCA1 ), affect the transcriptional regulation of ROS-responsive genes, ROS homeostasis, and tolerance to oxidative stress. Mis-expression of EARLY FLOWERING 3 , LUX ARRHYTHMO , and TIMING OF CAB EXPRESSION 1 affect ROS production and transcription, indicating a global effect of the clock on the ROS network. We propose CCA1 as a master regulator of ROS homeostasis through association with the Evening Element in promoters of ROS genes in vivo to coordinate time-dependent responses to oxidative stress. We also find that ROS functions as an input signal that affects the transcriptional output of the clock, revealing an important link between ROS signaling and circadian output. Temporal coordination of ROS signaling by CCA1 and the reciprocal control of circadian output by ROS reveal a mechanistic link that allows plants to master oxidative stress responses.

Early detection of salt stress is vital for plant survival and growth. Still, the molecular processes controlling early salt stress perception and signaling are not fully understood. Here, we identified salt-responsive ERF1 (SERF1), a rice (Oryza sativa) transcription factor (TF) gene that shows a root-specific induction upon salt and hydrogen peroxide (H2O2) treatment. Loss of SERF1 impairs the salt-inducible expression of genes encoding members of a mitogen-activated protein kinase (MAPK) cascade and salt tolerance-mediating TFs. Furthermore, we show that SERF1-dependent genes are H2O2 responsive and demonstrate that SERF1 binds to the promoters of MAPK kinase kinase6 (MAP3K6), MAPK5, dehydration-responsive element bindinG2A (DREB2A), and zinc finger protein179 (ZFP179) in vitro and in vivo. SERF1 also directly induces its own gene expression. In addition, SERF1 is a phosphorylation target of MAPK5, resulting in enhanced transcriptional activity of SERF1 toward its direct target genes. In agreement, plants deficient for SERF1 are more sensitive to salt stress compared with the wild type, while constitutive overexpression of SERF1 improves salinity tolerance. We propose that SERF1 amplifies the reactive oxygen species-activated MAPK cascade signal during the initial phase of salt stress and translates the salt-induced signal into an appropriate expressional response resulting in salt tolerance.

Leaf senescence is a highly dynamic process that has a major impact on crop production and quality.

Ethylene can only induce senescence in leaves that have reached a defined age. Thus, ethylene-induced senescence depends on age-related changes (ARCs) of individual leaves. The relationship between ethylene and age in the induction of leaf senescence was tested in Arabidopsis Ler-0, Col-0, and Ws-0 accessions as well as in eight old (onset of leaf death) mutants, isolated from the Ler-0 background. Plants with a constant final age of 24 d were exposed to ethylene for 3-16 d. The wild-type accessions showed a common response to the ethylene treatment. Increasing ethylene treatments of 3-12 d caused an increase in the number of yellow leaves. However, an ethylene exposure time of 16 d resulted in a decrease in the amount of yellowing. Thus, ethylene can both positively and negatively influence ARCs and the subsequent induction of leaf senescence, depending on the length of the treatment. The old mutants showed altered responses to the ethylene treatments. old1 and old11 were hypersensitive to ethylene in the triple response assay and a 12-d ethylene exposure resulted in a decrease in the amount of yellow leaves. The other six mutants did not show a decrease in yellow leaves with an ethylene treatment of 16 d. The results revealed that the effect of ethylene on the induction of senescence can be modified by at least eight genes.

The final size of an organism, or of single organs within an organism, depends on an intricate coordination of cell proliferation and cell expansion. Although organism size is of fundamental importance, the molecular and genetic mechanisms that control it remain far from understood. Here we identify a transcription factor, KUODA1 (KUA1), which specifically controls cell expansion during leaf development inArabidopsis thaliana. We show thatKUA1expression is circadian regulated and depends on an intact clock. Furthermore, KUA1 directly represses the expression of a set of genes encoding for peroxidases that control reactive oxygen species (ROS) homeostasis in the apoplast. Disruption ofKUA1results in increased peroxidase activity and smaller leaf cells. Chemical or genetic interference with the ROS balance or peroxidase activity affects cell size in a manner consistent with the identified KUA1 function. Thus, KUA1 modulates leaf cell expansion and final organ size by controlling ROS homeostasis.