Respiration in leaves and the continued elevation in the atmospheric
Plant steroid hormones brassinosteroids (
- NSF-PAR ID:
- 10371905
- Publisher / Repository:
- Wiley-Blackwell
- Date Published:
- Journal Name:
- The Plant Journal
- Volume:
- 100
- Issue:
- 5
- ISSN:
- 0960-7412
- Page Range / eLocation ID:
- p. 923-937
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Summary CO 2concentration causeCO 2‐mediated reduction in stomatal pore apertures. Several mutants have been isolated for which stomatal responses to both abscisic acid (ABA ) andCO 2are simultaneously defective. However, there are only few mutations that impair the stomatal response to elevatedCO 2, but not toABA . Such mutants are invaluable in unraveling the molecular mechanisms of earlyCO 2signal transduction in guard cells. Recently, mutations in the mitogen‐activated protein (MAP ) kinase, , have been shown to partially impairMPK 12CO 2‐induced stomatal closure. Here, we show thatmpk12 plants, in which is stably silenced specifically in guard cells (MPK 4mpk12 mpk4 homozygous double‐mutants), completely lackGC CO 2‐induced stomatal responses and have impaired activation of guard cell S‐type anion channels in response to elevatedCO 2/bicarbonate. However,ABA ‐induced stomatal closure, S‐type anion channel activation andABA ‐induced marker gene expression remain intact in thempk12 mpk4 double‐mutants. These findings suggest thatGC MPK 12 andMPK 4 act very early inCO 2signaling, upstream of, or parallel to the convergence ofCO 2andABA signal transduction. The activities ofMPK 4 andMPK 12 protein kinases were not directly modulated byCO 2/bicarbonatein vitro , suggesting that they are not directCO 2/bicarbonate sensors. Further data indicate thatMPK 4 andMPK 12 have distinguishable roles in Arabidopsis and that the previously suggested role ofRHC 1 in stomatalCO 2signaling is minor, whereasMPK 4 andMPK 12 act as key components of early stomatalCO 2signal transduction. -
Summary Mitogen‐activated protein kinase (
MPK ) cascades are conserved mechanisms of signal transduction across eukaryotes. Despite the importance ofMPK proteins in signaling events, specific roles for many ArabidopsisMPK proteins remain unknown. Multiple studies have suggested roles forMPK signaling in a variety of auxin‐related processes. To identifyMPK proteins with roles in auxin response, we screenedmpk insertional alleles and identifiedmpk1‐1 as a mutant that displays hypersensitivity in auxin‐responsive cell expansion assays. Further, mutants defective in the upstreamMAP kinase kinase MKK3 also display hypersensitivity in auxin‐responsive cell expansion assays, suggesting that thisMPK cascade affects auxin‐influenced cell expansion. We found that MPK1 interacts with and phosphorylates ROP BINDING PROTEIN KINASE 1 (RBK1), a protein kinase that interacts with members of the Rho‐like GTPases from Plants (ROP) small GTPase family. Similar tompk1‐1 andmkk3‐1 mutants,rbk1 insertional mutants display auxin hypersensitivity, consistent with a possible role for RBK1 downstream of MPK1 in influencing auxin‐responsive cell expansion. We found that RBK1 directly phosphorylates ROP4 and ROP6, supporting the possibility that RBK1 effects on auxin‐responsive cell expansion are mediated through phosphorylation‐dependent modulation of ROP activity. Our data suggest a MKK3 • MPK1 • RBK1 phosphorylation cascade that may provide a dynamic module for altering cell expansion. -
Abstract Brassinosteroids (
BRs ) are essential plant growth‐promoting hormones involved in many processes throughout plant development, from seed germination to flowering time. SinceBRs do not undergo long‐distance transport, cell‐ and tissue‐specific regulation of hormone levels involves both biosynthesis and inactivation. To date, tenBR ‐inactivating enzymes, with at least five distinct biochemical activities, have been experimentally identified in the model plantArabidopsis thaliana . Epigenetic interactions betweenT‐DNA insertion alleles and genetic linkage have hindered analysis of higher‐order null mutants in these genes. A previous study demonstrated that thebas1‐2 sob7‐1 ben1‐1 triple‐null mutant could not be characterized due to epigenetic interactions between the exonicT‐DNA insertions inbas1‐2 andsob7‐1, causing the intronicT‐DNA insertion ofben1‐1 to revert to a partial loss‐of‐function allele. We usedCRISPR‐Cas9 genome editing to avoid this problem and generated thebas1‐2 sob7‐1 ben1‐3 triple‐null mutant. This triple‐null mutant resulted in an additive seedling long‐hypocotyl phenotype. We also uncovered a role for ‐mediatedBEN1 BR ‐inactivation in seedling cotyledon petiole elongation that was not observed in the singleben1‐2 null mutant but only in the absence of both andBAS1 . In addition, genetic analysis demonstrated thatSOB7 does not contribute to the early‐flowering phenotype, whichBEN1 andBAS1 redundantly regulate. Our results show thatSOB7 ,BAS1 andBEN1 , have overlapping and independent roles based on their differential spatiotemporal tissue expression patternsSOB7 -
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ABA ), but underlying mechanisms remain elusive. Here, we report that the sole Arabidopsis heterotrimeric Gβ subunit,AGB 1, is required for four guard cell Caoresponses: induction of stomatal closure; inhibition of stomatal opening; [Ca2+]cytoscillation; and inositol 1,4,5‐trisphosphate (InsP3) production. Stomata in wild‐type Arabidopsis (Col) and in mutants of the canonical Gα subunit, , showed inhibition of stomatal opening and promotion of stomatal closure by Cao. By contrast, stomatal movements ofGPA 1agb1 mutants andagb1 /gpa1 double‐mutants, as well as those of theagg1agg2 Gγ double‐mutant, were insensitive to Cao. These behaviors contrast withABA ‐regulated stomatal movements, which involveGPA 1 andAGB 1/AGG 3 dimers, illustrating differential partitioning of G‐protein subunits among stimuli with similar ultimate impacts, which may facilitate stimulus‐specific encoding. knockouts retained reactive oxygen species andAGB 1NO production, but lostYC 3.6‐detected [Ca2+]cytoscillations in response to Cao, initiating only a single [Ca2+]cytspike. Experimentally imposed [Ca2+]cytoscillations restored stomatal closure inagb1 . Yeast two‐hybrid and bimolecular complementation fluorescence experiments revealed thatAGB 1 interacts with phospholipase Cs (PLCs), and Caoinduced InsP3 production in Col but not inagb1 . In sum, G‐protein signaling viaAGB 1/AGG 1/AGG 2 is essential for Cao‐regulation of stomatal apertures, and stomatal movements in response to Caoapparently require Ca2+‐induced Ca2+release that is likely dependent on Gβγ interaction withPLC s leading to InsP3 production.