Abstract
Background and AimsThe putative FASCICLIN-LIKE ARABINOGALACTAN PROTEIN 4 (At-FLA4) locus of Arabidopsis thaliana has previously been shown to be required for the normal growth of wild-type roots in response to moderately elevated salinity. However, the genetic and physiological pathway that connects At-FLA4 and normal root growth remains to be elucidated.MethodsThe radial swelling phenotype of At-fla4 was modulated with growth regulators and their inhibitors. The relationship of At-FLA4 to abscisic acid (ABA) signalling was analysed by probing marker gene expression and the observation of the At-fla4 phenotype in combination with ABA signalling mutants.Key ResultsApplication of ABA suppresses the non-redundant role of At-FLA4 in the salt response. At-FLA4 positively regulates the response to low ABA concentration in roots and is required for the normal expression of ABA- and abiotic stress-induced genes. The At-fla4 phenotype is enhanced in the At-abi4 background, while two genetic suppressors of ABA-induced gene expression are required for salt oversensitivity of At-fla4. Salt oversensitivity in At-fla4 is suppressed by the CYP707A inhibitor abscinazole E2B, and salt oversensitivity in At-fla4 roots is phenocopied by chemical inhibition of ABA biosynthesis.ConclusionsThe predicted lipid-anchored glycoprotein At-FLA4 positively regulates cell wall biosynthesis and root growth by modulating ABA signalling.
Highlights
Among the biopolymers of the plant cell wall, the vast group of hydroxyproline-rich glycoproteins (Showalter et al, 2010) comprises lightly glycosylated proline-rich proteins, moderately glycosylated extensins and highly glycosylated arabinogalactan-proteins (AGPs)
To define further the physiological process that is controlled by Aims The putative FASCICLIN-LIKE ARABINOGALACTAN PROTEIN 4 (At-FLA4), we tested the effect of growth regulators and other bioactive compounds on the At-fla4 mutant
The ‘core signalling pathway’ consists of PYRABACTIN RESISTANT 1/PYR1 LIKE (At-PYR1/PYL) proteins that are induced by abscisic acid (ABA) to bind to type 2C protein phosphatases (PP2Cs) such as At-ABI1, thereby releasing them from inhibiting SNF1-related protein kinases (SnRK2s)
Summary
Among the biopolymers of the plant cell wall, the vast group of hydroxyproline-rich glycoproteins (Showalter et al, 2010) comprises lightly glycosylated proline-rich proteins, moderately glycosylated extensins and highly glycosylated arabinogalactan-proteins (AGPs). Overexpression of the cotton orthologue of At-FLA12, named Gh-FLA1 (Liu et al, 2013), in transgenic cotton, results in an increased rate of fibre initiation and elongation and causes an upregulation of a suite of genes related to cell wall biosynthesis including other FLA genes, whereas antisense suppression has the opposite effect (Huang et al, 2013). This gain-of-function phenotype shows that FLAs can control the transcriptional programme for cell wall formation, which is best explained by a function in signalling. Salt oversensitivity in At-fla is suppressed by the CYP707A inhibitor abscinazole E2B, and salt oversensitivity in At-fla roots is phenocopied by chemical inhibition of ABA biosynthesis. † Conclusions The predicted lipid-anchored glycoprotein At-FLA4 positively regulates cell wall biosynthesis and root growth by modulating ABA signalling
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