MPK4-mediated phosphorylation of PHYTOCHROME INTERACTING FACTOR4 controls thermosensing by regulating histone variant H2A.Z deposition.

Plants can perceive a slight upsurge in ambient temperature and respond by undergoing morphological changes, such as elongated hypocotyls and early flowering. The dynamic functioning of PHYTOCHROME INTERACTING FACTOR4 (PIF4) in thermomorphogenesis is well established, although the complete regulatory pathway involved in thermosensing remains elusive. We establish that an increase in temperature from 22˚C to 28˚C induces upregulation and activation of MITOGEN-ACTIVATED PROTEIN KINASE 4 (MPK4) in Arabidopsis (Arabidopsis thaliana), subsequently leading to the phosphorylation of PIF4. Phosphorylated PIF4 represses the expression of ACTIN-RELATED PROTEIN 6 (ARP6), which is required for mediating the deposition of histone variant H2A.Z at its target loci. Furthermore, we demonstrate that variations in ARP6 expression in PIF4 phosphor-null and phosphor-mimetic seedlings affect hypocotyl growth at 22˚C and 28˚C by modulating the regulation of ARP6-mediated H2A.Z deposition at the loci of genes involved in elongating hypocotyl cells. Interestingly, the expression of MPK4 is also controlled by H2A.Z deposition in a temperature-dependent manner. Taken together, these findings highlight the regulatory mechanism of thermosensing by which MPK4-mediated phosphorylation of PIF4 affects ARP6-mediated H2A.Z deposition at the genes involved in hypocotyl cell elongation.

Phosphorylation of AGO1a by MAP kinases is required for miRNA mediated resistance against Xanthomonas oryzae pv. oryzae infection in rice.

Bacterial leaf blight is a devastating disease caused by Xanthomonas oryzae pv. oryzae (Xoo) which causes severe crop loss in rice. The molecular mechanism that initiates defense against such pathogens remains unexplored. Reports have suggested crucial role of several miRNAs in regulating immune responses in plants. Argonaute (AGO) proteins have been implicated in imparting immunity against pathogens by using small RNAs as guide molecules. Here, we show that phosphorylation of rice AGO1a by MAP kinases is required for miRNA expression regulation during Xoo infection. AGO1a is induced in response to pathogen infection and is under the control of SA signaling pathway. The pathogen responsive MAP kinases MPK3, MPK4 and MPK6, interact with AGO1a in planta and can phosphorylate the protein in vitro. Overexpression of AGO1a extends disease resistance against Xoo in rice and leads to a higher accumulation of miRNAs. Conversely, overexpression of a non phosphorylatable mutant protein aggravates disease susceptibility and remarkably suppresses the miRNA expression levels. At a molecular level, phosphorylation of AGO1a by MAP kinase is required for increased accumulation of miRNAs during pathogen challenge. Taken together, the data suggests that OsAGO1a is a direct phosphorylation target of MAP kinases and this phosphorylation is crucial for its role in imparting disease resistance.

Possible role of plant MAP kinases in the biogenesis and transcription regulation of rice microRNA pathway factors.

Signalling pathways play vital roles as determinants of almost all the molecular processes inside a eukaryotic cell. They are more often considered to be the link between extracellular and intracellular environmental cues. Gene silencing pathways have emerged to be involved in regulation of stress responses and developmental processes. However, very little is known about the crosstalk between signalling and silencing pathways and their influence on each other. The present work describes the effects of general protein kinase inhibitors and specific mitogen activated protein kinase (MAPK) pathway inhibitors on the components of microRNA pathway in rice. The kinase inhibitors significantly reduced the activities of miRNA biogenesis complex and changed the transcript expression of miRNA pathway factors. This study suggests a possible regulation of microRNA machinery by plant kinases and MAP kinases in particular.

Traversing the Links between Heavy Metal Stress and Plant Signaling.

Plants confront multifarious environmental stresses widely divided into abiotic and biotic stresses, of which heavy metal stress represents one of the most damaging abiotic stresses. Heavy metals cause toxicity by targeting crucial molecules and vital processes in the plant cell. One of the approaches by which heavy metals act in plants is by over production of reactive oxygen species (ROS) either directly or indirectly. Plants act against such overdose of metal in the environment by boosting the defense responses like metal chelation, sequestration into vacuole, regulation of metal intake by transporters, and intensification of antioxidative mechanisms. This response shown by plants is the result of intricate signaling networks functioning in the cell in order to transmit the extracellular stimuli into an intracellular response. The crucial signaling components involved are calcium signaling, hormone signaling, and mitogen activated protein kinase (MAPK) signaling that are discussed in this review. Apart from signaling components other regulators like microRNAs and transcription factors also have a major contribution in regulating heavy metal stress. This review demonstrates the key role of MAPKs in synchronously controlling the other signaling components and regulators in metal stress. Further, attempts have been made to focus on metal transporters and chelators that are regulated by MAPK signaling.