LEAFY and APETALA1/CAULIFLOWER have partially antagonistic activities in the control of floral initiation.

A fundamental question in biology is how organisms integrate the plethora of environmental cues that they perceive to trigger a coordinated response. The regulation of protein stability, which is largely mediated by the ubiquitin-proteasome system in eukaryotes, plays a pivotal role in these processes. Due to their sessile lifestyle and the need to respond rapidly to a multitude of environmental factors, plants are thought to be especially dependent on proteolysis to regulate cellular processes. In this review, we present the complexity of the ubiquitin system in plants, and discuss the relevance of the proteolytic and non-proteolytic roles of this system in the regulation and coordination of plant responses to environmental signals. We also discuss the role of the ubiquitin system as a key regulator of plant signaling pathways. We focus more specifically on the functions of E3 ligases as regulators of the jasmonic acid (JA), salicylic acid (SA) and ethylene hormone signaling pathways that play important roles to mount a coordinated response to multiple environmental stresses. We also provide examples of new players in this field that appear to integrate different cues and signaling pathways.

To efficiently counteract pathogens, plants rely on a complex set of immune responses that are tightly regulated to allow the timely activation, appropriate duration and adequate amplitude of defense programs. The coordination of the plant immune response is known to require the activity of the ubiquitin/proteasome system, which controls the stability of proteins in eukaryotes. Here, we demonstrate that the N-end rule pathway, a subset of the ubiquitin/proteasome system, regulates the defense against a wide range of bacterial and fungal pathogens in the model plantArabidopsis thaliana. We show that this pathway positively regulates the biosynthesis of plant-defense metabolites such as glucosinolates, as well as the biosynthesis and response to the phytohormone jasmonic acid, which plays a key role in plant immunity. Our results also suggest that the arginylation branch of the N-end rule pathway regulates the timing and amplitude of the defense program against the model pathogenPseudomonas syringaeAvrRpm1.

The gene regulatory network comprised of LEAFY (LFY), APETALA1 (AP1), the AP1 paralog CAULIFLOWER (CAL), and TERMINAL FLOWER1 (TFL1) is a major determinant of the flowering process in Arabidopsis thaliana. TFL1 activity in the shoot apical meristem provides inflorescence identity while the transcription factors LFY and AP1/CAL confer floral identity to emerging floral primordia. It has been thought that LFY and AP1/CAL control the onset of flowering in part by repressing TFL1 expression in flowers. However, in the June issue of Plant Physiology, we reported that LFY and AP1 act antagonistically in the regulation of several key flowering regulators, including TFL1. Specifically, TFL1 transcription was suppressed by AP1 but promoted by LFY. Here, we present additional evidence for the role of LFY as an activator of TFL1 and propose that this regulatory activity is pivotal for the indeterminate growth of the SAM during the reproductive phase of development.

In plants, the protein RPM1-INTERACTING PROTEIN4 (RIN4) is a central regulator of both pattern-triggered immunity and effector-triggered immunity. RIN4 is targeted by several effectors, including the Pseudomonas syringae protease effector AvrRpt2. Cleavage of RIN4 by AvrRpt2 generates potentially unstable RIN4 fragments, whose degradation leads to the activation of the resistance protein RESISTANT TO P. SYRINGAE2. Hence, identifying the determinants of RIN4 degradation is key to understanding RESISTANT TO P. SYRINGAE2–mediated effector-triggered immunity, as well as virulence functions of AvrRpt2. In addition to RIN4, AvrRpt2 cleaves host proteins from the nitrate-induced (NOI) domain family. Although cleavage of NOI domain proteins by AvrRpt2 may contribute to pattern-triggered immunity regulation, the (in)stability of these proteolytic fragments and the determinants regulating their stability remain unexamined. Notably, a common feature of RIN4, and of many NOI domain protein fragments generated by AvrRpt2 cleavage, is the exposure of a new N-terminal residue that is destabilizing according to the N-end rule. Using antibodies raised against endogenous RIN4, we show that the destabilization of AvrRpt2-cleaved RIN4 fragments is independent of the N-end rule pathway (recently renamed the N-degron pathway). By contrast, several NOI domain protein fragments are genuine substrates of the N-degron pathway. The discovery of this set of substrates considerably expands the number of known proteins targeted for degradation by this ubiquitin-dependent pathway in plants. These results advance our current understanding of the role of AvrRpt2 in promoting bacterial virulence.

MADS-domain transcription factors are involved in the control of a multitude of processes in eukaryotes, and in plants, they play particularly important roles during reproductive development. Among the members of this large family of regulatory proteins are the floral organ identity factors, which specify the identities of the different types of floral organs in a combinatorial manner. Much has been learned over the past three decades about the function of these master regulators. For example, it has been shown that they have similar DNA-binding activities and that their genome-wide binding patterns exhibit large overlaps. At the same time, it appears that only a minority of binding events lead to changes in gene expression and that the different floral organ identity factors have distinct sets of target genes. Thus, binding of these transcription factors to the promoters of target genes alone may not be sufficient for their regulation. How these master regulators achieve specificity in a developmental context is currently not well understood. Here, we review what is known about their activities and highlight open questions that need to be addressed to gain more detailed insights into the molecular mechanisms underlying their functions. We discuss evidence for the involvement of cofactors as well as the results from studies on transcription factors in animals that may be instructive for a better understanding of how the floral organ identity factors achieve regulatory specificity.