Pectins, major components of dicot cell walls, are synthesized in a heavily methylesterified form in the Golgi and are partially deesterified by pectin methylesterases (PMEs) upon export to the cell wall. PME activity is important for the virulence of the necrotrophic fungal pathogen Botrytis cinerea. Here, the roles of Arabidopsis PMEs in pattern-triggered immunity and immune responses to the necrotrophic fungus Alternaria brassicicola and the bacterial hemibiotroph Pseudomonas syringae pv maculicola ES4326 (Pma ES4326) were studied. Plant PME activity increased during pattern-triggered immunity and after inoculation with either pathogen. The increase of PME activity in response to pathogen treatment was concomitant with a decrease in pectin methylesterification. The pathogen-induced PME activity did not require salicylic acid or ethylene signaling, but was dependent on jasmonic acid signaling. In the case of induction by A. brassicicola, the ethylene response factor, but not the MYC2 branch of jasmonic acid signaling, contributed to induction of PME activity, whereas in the case of induction by Pma ES4326, both branches contributed. There are 66 PME genes in Arabidopsis, suggesting extensive genetic redundancy. Nevertheless, selected pme single, double, triple and quadruple mutants allowed significantly more growth of Pma ES4326 than wild-type plants, indicating a role of PMEs in resistance to this pathogen. No decreases in total PME activity were detected in these pme mutants, suggesting that the determinant of immunity is not total PME activity; rather, it is some specific effect of PMEs such as changes in the pattern of pectin methylesterification.The plant cell wall determines cell shape, facilitates cell-cell interaction, and provides mechanical strength to plant cells. De Bary (1886) first observed that a plant pathogen, Sclerotina sclerotiorum, degraded host cell walls during infection. Later, it was concluded that plant cell walls act as preformed structural barriers against pathogen entry, because it was noticed that many plant pathogens produced various types of cell wall-degrading enzymes and that some of those were required for optimal infection of host plants (Albersheim et al., 1969).Arabidopsis mesophyll cells are surrounded by primary cell walls consisting of three major components: cellulose, hemicelluloses, and pectins. Pectins make up approximately 50% of Arabidopsis leaf cell walls (Zablackis et al., 1995;Harholt et al., 2010). They are complex GalA-containing polysaccharides composed of homogalacturonan (HG), rhamnogalacturonan I and II, and xylogalacturonan (Mohnen, 2008). HG is typically the most abundant polysaccharide, constituting approximately 65% of the pectin (Mohnen, 2008;Harholt et al., 2010). HG is a linear homopolymer of 1,4-linked GalA and is synthesized in the Golgi in a highly methylesterified form (Caffall and Mohnen, 2009). Pectin methylesterases (PMEs) demethylesterify HG in the apoplast (Mohnen, 2008;Harholt et al., 2010). Demethylesterification of pectin is considered t...
Summary In this paper we describe PATTERN‐TRIGGERED IMMUNITY (PTI) COMPROMISED RECEPTOR‐LIKE CYTOPLASMIC KINASE 1 (PCRK1) of Arabidopsis thaliana, an RLCK that is important for defense against the pathogen Pseudomonas syringae pv. maculicola ES4326 (Pma ES4326). We examined defense responses such as bacterial growth, production of reactive oxygen species (ROS) and callose deposition in pcrk1 mutant plants to determine the role of PCRK1 during pathogen infection. Expression of PCRK1 was induced following pathogen infection. Pathogen growth was significantly higher in pcrk1 mutant lines than in wild‐type Col‐0. Mutant pcrk1 plants showed reduced pattern‐triggered immunity (PTI) against Pma ES4326 after pretreatment with peptides derived from flagellin (flg22), elongation factor‐Tu (elf18), or an endogenous protein (pep1). Deposition of callose was reduced in pcrk1 plants, indicating a role of PCRK1 in activation of early immune responses. A PCRK1 transgene containing a mutation in a conserved lysine residue important for phosphorylation activity of kinases (K118E) failed to complement a pcrk1 mutant for the Pma ES4326 growth phenotype. Our study shows that PCRK1 plays an important role during PTI and that a conserved lysine residue in the putative kinase domain is important for PCRK1 function.
Key messageThree adjacent and distinct sequence rearrangements were identified at a NAP1 locus in a soybean mutant. Genetic dissection and validation revealed the function of this gene in soybean trichome development.AbstractA soybean (Glycine max (L.) Merr.) gnarled trichome mutant, exhibiting stunted trichomes compared to wild-type, was identified in a fast neutron mutant population. Genetic mapping using whole genome sequencing-based bulked segregant analysis identified a 26.6 megabase interval on chromosome 20 that co-segregated with the phenotype. Comparative genomic hybridization analysis of the mutant indicated that the chromosome 20 interval included a small structural variant within the coding region of a soybean ortholog (Glyma.20G019300) of Arabidopsis Nck-Associated Protein 1 (NAP1), a regulator of actin nucleation during trichome morphogenesis. Sequence analysis of the candidate allele revealed multiple rearrangements within the coding region, including two deletions (approximately 1–2 kb each), a translocation, and an inversion. Further analyses revealed that the mutant allele perfectly co-segregated with the phenotype, and a wild-type soybean NAP1 transgene functionally complemented an Arabidopsis nap1 mutant. In addition, mapping and exon sequencing of NAP1 in a spontaneous soybean gnarled trichome mutant (T31) identified a frame shift mutation resulting in a truncation of the coding region. These data indicate that the soybean NAP1 gene is essential for proper trichome development and show the utility of the soybean fast neutron population for forward genetic approaches for identifying genes.Electronic supplementary materialThe online version of this article (doi:10.1007/s00122-016-2735-x) contains supplementary material, which is available to authorized users.
Early canopy coverage is a desirable trait that promotes faster ground coverage, resulting in reduced soil evaporation, increased light interception, biomass production and weed suppression, all of which are important determinants of yield in soybean (Glycine max). Variation in traits comprising shoot architecture can in uence canopy coverage, canopy light interception, canopy-level photosynthesis, and source-sink partitioning e ciency. However, little is known about the extent of phenotypic diversity of shoot architecture traits and their genetic control in soybean. Thus, we sought to understand the contribution of shoot architecture traits to canopy coverage and to determine the genetic control of these traits. We examined the natural variation for shoot architecture traits in a set of 399 diverse maturity group I soybean (SoyMGI) accessions to identify relationships between traits, and to identify loci that are associated with canopy coverage and shoot architecture traits. Canopy coverage was correlated with branch angle, number of branches, plant height and leaf shape. Using previously collected 50K SNP data on the SoyMGI panel, we identi ed QTL associated with branch angle, number of branches, branch density, leaf length/width ratio, days to owering, maturity, plant height, number of nodes and stem termination. In many cases QTL intervals overlapped with previously described genes or QTL. Of particular note, we found QTL associated with branch angle and lea et shape located on chromosomes 19 and 4, respectively, and these QTL overlapped with QTL associated with canopy coverage, suggesting the importance of branch angle and lea et shape in determining canopy coverage. Taken together, our results highlight the role individual architecture traits play in canopy coverage and contribute information on their genetic control that could help facilitate future efforts in their genetic manipulation.
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