Unable to rescue disruption phenotype. Ectopic stomata formation and increased accumulation; when associated with A-211, A-214, A-219 and A-255. Ectopic asymmetric cell divisions, but fails to produce stomata, and reduced repression by osmotic stress (e.g. mannitol); when associated with A-211, A-214 and A-219.
In rid2-1; temperature-sensitive mutant with altered reactivation of cell proliferation in the hypocotyl stele during callus formation from hypocotyl and root explants above 28 degrees Celsius. Impaired initiation of lateral root primordia formation. Exhibits abnormalities in the formation of the root apical meristem (RAM). Various (acute and non-acute) temperature sensitive inhibitory effects on different aspects of cell proliferation leading to reduced roots and leaves development during seedling growth. Nucleolar vacuolation and excessive accumulation of various intermediates of pre-rRNA processing. Abnormally swollen cells during culture on callus-inducing medium (CIM) with extraordinarily large nucleoli.
Increased sensitivity to the pathogenic biotrophic bacteria Xanthomonas campestris pv. campestris (Xcc) in vascular tissues. Lost ability to trigger cell death in response to the Xanthomonas campestris effector XopAC/AvrAC in the presence of PBL2 and RKS1. Impaired Xanthomonas campestris effector AvrAC/XopAC-mediated uridylylation; when associated with A-254.
Increased sensitivity to the pathogenic biotrophic bacteria Xanthomonas campestris pv. campestris (Xcc) in vascular tissues. Lost ability to trigger cell death in response to the Xanthomonas campestris effector XopAC/AvrAC in the presence of PBL2 and RKS1. Impaired Xanthomonas campestris effector AvrAC/XopAC-mediated uridylylation; when associated with A-253.
In alt2-1; severely sensitive to the intrastrand DNA cross-linking agent cisplatin (CDDP) and to the DNA cross-linking agent mitomycin C (MMC), enhanced tolerance to aluminum (Al), but impaired halting root growth in response to Al toxicity. Fails to halt cell cycle progression in the presence of DNA cross-linking agents.
In osz2; semi-dominant mutation with impaired proteolytic processing, and leading to an increased sensitivity to zinc Zn(2+) characterized by Zn-triggered reduced root elongation due to a defect in cell elongation, but an increase number of root hairs; this phenotype is suppressed by calcium Ca(2+) treatment. No obvious impact on pectin methylesterification.
In BASL_123456D; phosphomimetic, increased interaction with YDA and promoted polarization; when associated with D-89, D-145, D-168, D-235 and D-246. In BASL_14D; reduced mobility leading to severely retarded recovery at the cell cortex and prolonged accumulation even in mature pavement cells, and impaired stomatal production due to suppressed SLGC division potential; when associated with D-89.
In BASL_123456D; phosphomimetic, increased interaction with YDA and promoted polarization; when associated with D-72, D-145, D-168, D-235 and D-246. In BASL_14D; reduced mobility leading to severely retarded recovery at the cell cortex and prolonged accumulation even in mature pavement cells, and impaired stomatal production due to suppressed SLGC division potential; when associated with D-72.
In crl-2; impeded plastid division leading to enlarged chloroplasts in mesophyll cells and abnormal plastid homeostasis, thus resulting in preconditioning plants by activating the expression of stress genes, enhancing pathogen resistance (e.g. Pseudomonas syringae DC3000) and attenuating the capacity to respond to plastid signals. Spontaneous light intensity-dependent cell death formation associated with O(2) production.
In spch-5; normal growth, but extremely low number of sometimes clustered stomata in leaves and stomata free hypocotyls due to decreased ability to initiate and amplify lineages, defects in asymmetric cell fate allocation, and misorientation of asymmetric division planes. These phenotypes are partly rescued by brassinosteroids (BRs) by rescuing the expression of a set of target genes.
In chs1-1 and chs1-2; Increased leaves sensitivity to chilling stress in an EDS1- and PAD4-dependent manner, killed by several days of exposure to temperatures below 18 degrees Celsius. Alterations in photosynthetic complexes, chloroplast ultrastructure, and thylakoid membrane integrity and lipid composition precede leaf cell death. Leaf chlorosis and electrolyte leakage after exposure to chilling temperatures associated with abnormal steryl-esters accumulation and reduced sterols levels. Chilling leads to xanthophyll cycle activation and accumulation of tocopherol. Activation of immune responses by chilling; increased salicylic acid (SA) and hydrogen peroxide H(2)O(2) production, extensive cell death and pathogenesis-related (PR) genes expression at 13 degrees Celsius. Massive necrotic response to virulent Pseudomonas syringae pv. tomato infection, but normal bacterial proliferation. Increased permeability to boric acid.
In zed1-D; normal growth of plants grown below 22 degrees Celsius, but high temperature (above 22 degrees Celsius)-dependent RPP13L4/ZAR1-influenced autoimmunity and growth retardation. Plants cultivated above 23 degrees Celsius are dwarf with crinkled lamina, shortened petiole, reduced pedicel length and silique numbers, increased branches, severely shortened inflorescence stem and clustered siliques. These phenotypes are associated with inhibited cell elongation and/or expansion and disturbed differentiation of trichomes and stomata, disorganized interfascicular fibers and fewer pith tissues in inflorescence stems as well as increased lignin deposition in the vasculatures. Elevated reactive oxygen species (ROS) content and extensive cell death as well as reduced expression of pathogenesis related genes (e.g. PR1 and PR2) but accumulation of SNC1 when grown at 25 degrees Celsius. The high temperature-induced autoimmune phenotype is blocked in the double mutant zed1-D zar1-3. Stronger binding activity with RPP13L4/ZAR1. Confined to the cytosol. Fully rescued by the over-expression of RKS1/ZRK1 and ZRK12, and partially by the over-expression of ZRK4, ZRK10, ZRK13 and ZRK14. The double mutants zed1-D snc1-11 and zed1-D nahG have restored normal growth phenotypes and rescued autoimmunity defects. These pleiotropic phenotypes are suppressed in plants lacking SZE1 and SZE2.
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