ROS signaling: the new wave?

Reactive oxygen species (ROS) play an integral role as signalling molecules in the regulation of numerous biological processes such as growth, development, and responses to biotic and/or abiotic stimuli in plants. To some extent, various functions of ROS signalling are attributed to differences in the regulatory mechanisms of respiratory burst oxidase homologues (RBOHs) that are involved in a multitude of different signal transduction pathways activated in assorted tissue and cell types under fluctuating environmental conditions. Recent findings revealed that stress responses in plants are mediated by a temporal-spatial coordination between ROS and other signals that rely on production of stress-specific chemicals, compounds, and hormones. In this review we will provide an update of recent findings related to the integration of ROS signals with an array of signalling pathways aimed at regulating different responses in plants. In particular, we will address signals that confer systemic acquired resistance (SAR) or systemic acquired acclimation (SAA) in plants.

ROS as key players in plant stress signalling

Ca(2+) signals are core transducers and regulators in many adaptation and developmental processes of plants. Ca(2+) signals are represented by stimulus-specific signatures that result from the concerted action of channels, pumps, and carriers that shape temporally and spatially defined Ca(2+) elevations. Cellular Ca(2+) signals are decoded and transmitted by a toolkit of Ca(2+) binding proteins that relay this information into downstream responses. Major transduction routes of Ca(2+) signaling involve Ca(2+)-regulated kinases mediating phosphorylation events that orchestrate downstream responses or comprise regulation of gene expression via Ca(2+)-regulated transcription factors and Ca(2+)-responsive promoter elements. Here, we review some of the remarkable progress that has been made in recent years, especially in identifying critical components functioning in Ca(2+) signal transduction, both at the single-cell and multicellular level. Despite impressive progress in our understanding of the processing of Ca(2+) signals during the past years, the elucidation of the exact mechanistic principles that underlie the specific recognition and conversion of the cellular Ca(2+) currency into defined changes in protein-protein interaction, protein phosphorylation, and gene expression and thereby establish the specificity in stimulus response coupling remain to be explored.

https://www.jstor.org/stable/info/25680077

Calcium signals: the lead currency of plant information processing

Plants depend on cell-autonomous innate immune mechanisms for protection against infection and these pathways are activated in response to pattern recognition receptor (PRR) engagement. However, as is the case in mammals, PRR signalling in plants must be tightly controlled to avoid pathological outcomes; this Review focuses on the mechanisms that regulate plant PRR signalling.

Regulation of pattern recognition receptor signalling in plants.

http://biol.unt.edu/~rmittler/Papers/Respiratory%20burst%20oxidases%20The%20engines%20of%20ROS%20signaling.pdf

Respiratory burst oxidases: the engines of ROS signaling.

Synergistic Activation of the Arabidopsis NADPH Oxidase AtrbohD by Ca2+ and Phosphorylation

Identification of putative voltage-dependent Ca2+-permeable channels involved in cryptogein-induced Ca2+ transients and defense responses in tobacco BY-2 cells.

To gain insight into the cellular functions of the mid1-complementing activity (MCA) family proteins, encoding putative Ca2+-permeable mechanosensitive channels, we isolated two MCA homologs of tobacco (Nicotiana tabacum) BY-2 cells, named NtMCA1 and NtMCA2. NtMCA1 and NtMCA2 partially complemented the lethality and Ca2+ uptake defects of yeast mutants lacking mechanosensitive Ca2+ channel components. Furthermore, in yeast cells overexpressing NtMCA1 and NtMCA2, the hypo-osmotic shock-induced Ca2+ influx was enhanced. Overexpression of NtMCA1 or NtMCA2 in BY-2 cells enhanced Ca2+ uptake, and significantly alleviated growth inhibition under Ca2+ limitation. NtMCA1-overexpressing BY-2 cells showed higher sensitivity to hypo-osmotic shock than control cells, and induced the expression of the touch-inducible gene, NtERF4. We found that both NtMCA1-GFP and NtMCA2-GFP were localized at the plasma membrane and its interface with the cell wall, Hechtian strands, and at the cell plate and perinuclear vesicles of dividing cells. NtMCA2 transcript levels fluctuated during the cell cycle and were highest at the G1 phase. These results suggest that NtMCA1 and NtMCA2 play roles in Ca2+-dependent cell proliferation and mechanical stress-induced gene expression in BY-2 cells, by regulating the Ca2+ influx through the plasma membrane.

Involvement of the putative Ca 2+ -permeable mechanosensitive channels, NtMCA1 and NtMCA2, in Ca 2+ uptake, Ca 2+ -dependent cell proliferation and mechanical stress-induced gene expression in tobacco ( Nicotiana tabacum ) BY-2 cells

To provide insights into the mechanisms by which receptors for pathogenic elicitors activate defense signaling, we investigated the duration of cryptogein treatment required for induction of various defense responses including programmed cell death in synchronized tobacco BY-2 cells. Transient cryptogein treatment induced only a rapid and transient phase of oxidative burst and mitogen-activated protein kinase (MAPK) activation. Prolonged production

/pdf/continuous-recognition-of-the-elicitor-signal-for-several-4u551j6edp.pdf

Continuous recognition of the elicitor signal for several hours is prerequisite for induction of cell death and prolonged activation of signaling events in tobacco BY-2 cells.

Yoko Ogasawara

Papers

Synergistic Activation of the Arabidopsis NADPH Oxidase AtrbohD by Ca2+ and Phosphorylation

Identification of putative voltage-dependent Ca2+-permeable channels involved in cryptogein-induced Ca2+ transients and defense responses in tobacco BY-2 cells.

Involvement of the putative Ca 2+ -permeable mechanosensitive channels, NtMCA1 and NtMCA2, in Ca 2+ uptake, Ca 2+ -dependent cell proliferation and mechanical stress-induced gene expression in tobacco ( Nicotiana tabacum ) BY-2 cells

Continuous recognition of the elicitor signal for several hours is prerequisite for induction of cell death and prolonged activation of signaling events in tobacco BY-2 cells.