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The phytohormone cytokinin plays a significant role in nearly all aspects of plant growth and development. Cytokinin signaling has primarily been studied in the dicot model Arabidopsis, with relatively little work done in monocots, which include rice (Oryza sativa) and other cereals of agronomic importance. The cytokinin signaling pathway is a phosphorelay comprised of the histidine kinase receptors, the authentic histidine phosphotransfer proteins (AHPs) and type‐B response regulators (RRs). Two negative regulators of cytokinin signaling have been identified: the type‐A RRs, which are cytokinin primary response genes, and the pseudo histidine phosphotransfer proteins (PHPs), which lack the His residue required for phosphorelay. Here, we describe the role of the ricePHPgenes. Phylogenic analysis indicates that the PHPs are generally first found in the genomes of gymnosperms and that they arose independently in monocots and dicots. Consistent with this, the three ricePHPsfail to complement an Arabidopsisphpmutant (aphp1/ahp6). Disruption of the three ricePHPsresults in a molecular phenotype consistent with these elements acting as negative regulators of cytokinin signaling, including the induction of a number of type‐A RR and cytokinin oxidase genes. The triplephpmutant affects multiple aspects of rice growth and development, including shoot morphology, panicle architecture, and seed fill. In contrast to Arabidopsis, disruption of the ricePHPsdoes not affect root vascular patterning, suggesting that while many aspects of key signaling networks are conserved between monocots and dicots, the roles of at least some cytokinin signaling elements are distinct.

 

The phytohormone cytokinin influences many aspects of plant growth and development, several of which also involve the cellular process of autophagy, including leaf senescence, nutrient remobilization, and developmental transitions. TheArabidopsistype-A response regulators (type-A ARR) are negative regulators of cytokinin signaling that are transcriptionally induced in response to cytokinin. Here, we describe a mechanistic link between cytokinin signaling and autophagy, demonstrating that plants modulate cytokinin sensitivity through autophagic regulation of type-A ARR proteins. Type-A ARR proteins were degraded by autophagy in an AUTOPHAGY-RELATED (ATG)5-dependent manner, and this degradation is promoted by phosphorylation on a conserved aspartate in the receiver domain of the type-A ARRs. EXO70D family members interacted with type-A ARR proteins, likely in a phosphorylation-dependent manner, and recruited them to autophagosomes via interaction of the EXO70D AIM with the core autophagy protein, ATG8. Consistently, loss-of-functionexo70D1,2,3mutants exhibited compromised targeting of type-A ARRs to autophagic vesicles, have elevated levels of type-A ARR proteins, and are hyposensitive to cytokinin. Disruption of both type-AARRsandEXO70D1,2,3compromised survival in carbon-deficient conditions, suggesting interaction between autophagy and cytokinin responsiveness in response to stress. These results indicate that the EXO70D proteins act as selective autophagy receptors to target type-A ARR cargos for autophagic degradation, demonstrating modulation of cytokinin signaling by selective autophagy.

 

Cytokinin is an important phytohormone that employs a multistep phosphorelay to transduce the signal from receptors to the nucleus, culminating in activation of type-B response regulators which function as transcription factors. Recent chromatin immunoprecipitation-sequencing (ChIP-seq) studies have identified targets of type-B ARABIDOPSIS RESPONSE REGULATORs (ARRs) and integrated these into the cytokinin-activated transcriptional network. Primary targets of the type-B ARRs are enriched for genes involved in hormonal regulation, emphasizing the extensive crosstalk that can occur between cytokinin, auxin, abscisic acid, brassinosteroids, gibberellic acid, ethylene, jasmonic acid, and salicylic acid. Examination of hormone-related targets reveals multiple regulatory points including biosynthesis, degradation/inactivation, transport, and signal transduction. Here, we consider this early response to cytokinin in terms of the hormones involved, points of regulatory crosstalk, and physiological significance.