A mutation in the cytosolic O-acetylserine (thiol) lyase induces a genome-dependent early leaf death phenotype in Arabidopsis

Background: Cysteine is a component in organic compounds including glutathione that have been implicated in the adaptation of plants to stresses. O-acetylserine (thiol) lyase (OAS-TL) catalyses the final step of cysteine biosynthesis. OAS-TL enzyme isoforms are localised in the cytoplasm, the plastids and mitochondria but the contribution of individual OAS-TL isoforms to plant sulphur metabolism has not yet been fully clarified. Results: The seedling lethal phenotype of the Arabidopsis onset of leaf death3-1 (old3-1) mutant is due to a point mutation in the OAS-A1 gene, encoding the cytosolic OAS-TL. The mutation causes a single amino acid substitution from Gly162 to Glu162, abolishing old3-1 OAS-TL activity in vitro. The old3-1 mutation segregates as a monogenic semi-dominant trait when backcrossed to its wild type accession Landsberg erecta (Ler-0) and the Di-2 accession. Consistent with its semi-dominant behaviour, wild type Ler-0 plants transformed with the mutated old3-1 gene, displayed the early leaf death phenotype. However, the old3-1 mutation segregates in an 11:4:1 (wild type: semi-dominant: mutant) ratio when backcrossed to the Colombia-0 and Wassilewskija accessions. Thus, the early leaf death phenotype depends on two semi-dominant loci. The second locus that determines the old3-1 early leaf death phenotype is referred to as odd-ler (for old3 determinant in the Ler accession) and is located on chromosome 3. The early leaf death phenotype is temperature dependent and is associated with increased expression of defence-response and oxidative-stress marker genes. Independent of the presence of the odd-ler gene, OAS-A1 is involved in maintaining sulphur and thiol levels and is required for resistance against cadmium stress. Conclusions: The cytosolic OAS-TL is involved in maintaining organic sulphur levels. The old3-1 mutation causes genome-dependent and independent phenotypes and uncovers a novel function for the mutated OAS-TL in cell death regulation.

The contribution of SERF1 to root-to-shoot signaling during salinity stress in rice

Stress perception and communication play important roles in the adaptation of plants to changing environmental conditions. Plant roots are the first organs to detect changes in the soil water potential induced by salt stress. In the presence of salinity stress, root-to-shoot communication occurs to adjust the growth of the whole plant. So far, the phytohormone abscisic acid (ABA), hydraulic signals and reactive oxygen species (ROS) have been proposed to mediate this communication under salt stress. Recently, we identified the rice transcription factor SALT-RESPONSIVE ERF1 (SERF1), which regulates a ROS-dependent transcriptional cascade in roots required for salinity tolerance. Upon salt stress, SERF1 knockout mutant plants show an increased leaf temperature as compared with wild type. As this occurs within the first 20 min of salt stress, we here evaluated the involvement of SERF1 in the perception of salt stress in the shoot. By metabolic profiling and expression analysis we show that the action of SERF1 in signal communication to the shoot is independent from ABA, but does affect the accumulation of ROS-related metabolites and transcripts under short-term salt stress

The contribution of SERF1 to root-to-shoot signaling during salinity stress in rice

Schmidt R, Caldana C, Mueller-Roeber B, Schippers JHM. The contribution of SERF1 to root-to-shoot signaling during salinity stress in rice. Plant Signaling & Behavior. 2014;9(1): e27540

Functional Consequences of Toll-like Receptor 4 Polymorphisms

Toll-like receptor 4 (TLR4) is an important pathogen recognition receptor that recognizes mainly lipopolysaccharide (LPS) of Gram-negative bacteria, but also structures from fungal and mycobacterial pathogens, as well as endogenous ligands. Two nonsynonymous polymorphisms of TLR4, Asp299Gly and Thr399Ile, have been suggested to alter the function of the receptor. Some, but not all, studies have proposed that these polymorphisms lead to reduced cytokine response and increased susceptibility to Gram-negative infections. In this review, we compare studies that assessed the effect of the Asp299Gly and Thr399Ile polymorphisms on susceptibility to Gram-negative infections and examine the phenotypic consequences of these polymorphisms. In addition, we review the geographical distribution of TLR4 polymorphisms and present a model for evolutionary pressures on the TLR4 genetic make-up