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.

Kauri ( Agathis australis ), which is one of the world's largest and longest‐living conifer species, is under threat from a root and collar dieback disease caused by the oomycete pathogen Phytophthora agathidicida . The noted incidence of kauri dieback has increased in the past decade, and even trees >1000 years old are not immune. This disease has profound effects on both forest ecosystems and human society, particularly indigenous Māori, for whom kauri is a taonga or treasure of immense significance. This review brings together existing scientific knowledge about the pathogen and the devastating disease it causes, as well as highlighting important knowledge gaps and potential approaches for disease management. The life cycle of P. agathidicida is similar to those of other soilborne Phytophthora pathogens, with roles for vegetative hyphae, zoospores and oospores in the disease. However, there is comparatively little known about many aspects of the biology of P. agathidicida , such as its host range and disease latency, or about the impact on the disease of abiotic and biotic factors such as soil health and co‐occurring Phytophthora species. This review discusses current and emerging tools and strategies for surveillance, diagnostics and management, including a consideration of genomic resources, and the role these play in understanding the pathogen and how it causes this deadly disease. Key aspects of indigenous Māori knowledge, which include rich ecological and historical knowledge of kauri forests and a holistic approach to forest health, are highlighted.

Leaf senescence in Arabidopsis thaliana is a strict, genetically controlled nutrient recovery program, which typically progresses in an age-dependent manner. Leaves of the Arabidopsis onset of leaf death5 (old5) mutant exhibit early developmental senescence. Here, we show that OLD5 encodes quinolinate synthase (QS), a key enzyme in the de novo synthesis of NAD. The Arabidopsis QS was previously shown to carry a Cys desulfurase domain that stimulates reconstitution of the oxygen-sensitive Fe-S cluster that is required for QS activity. The old5 lesion in this enzyme does not affect QS activity but it decreases its Cys desulfurase activity and thereby the long-term catalytic competence of the enzyme. The old5 mutation causes increased NAD steady state levels that coincide with increased activity of enzymes in the NAD salvage pathway. NAD plays a key role in cellular redox reactions, including those of the tricarboxylic acid cycle. Broad-range metabolite profiling of the old5 mutant revealed that it contains higher levels of tricarboxylic acid cycle intermediates and nitrogen-containing amino acids. The mutant displays a higher respiration rate concomitant with increased expression of oxidative stress markers. We postulate that the alteration in the oxidative state is integrated into the plant developmental program, causing early ageing of the mutant.