The identification and characterization of seedlings hyper-responsive to light 2 (SHL2), a gene implicated in developmental responses to light

• Main Author: Seong, Mi-Seon
• Other Authors: Pepper, Alan E
• Format: Others
• Language: en_US
• Published: Texas A&M University 2007
• Subjects: Seedlings Hyper-responsive to Light 2; SHL2; Light; hypocotyl; Xyloglucan galactosyltransferase; cell wall; Arabidopsis
• Online Access: http://hdl.handle.net/1969.1/4764

Mutants showing developmental hyper-responsiveness to limited light were screened and designated as seedlings hyper-responsive to light (shl). These mutants showed an etiolated phenotype similar to wild type in the dark, yet had shorter hypocotyls, larger cotyledons, and more advanced development of true leaves than wild type in low light. The SHL genes act (genetically) as light-dependent negative regulators of photomorphogenesis, possibly in a downstream signaling or developmental pathway that is shared by the major photoreceptor genes (CRY1, PHYA, and PHYB) and other photoreceptors (CRY2, PHYC, PHYD, and PHYE). shl1 and shl2 were shown to be partially dependent on HY5 activity for their light-hyperresponsive phenotypes. shl1-1 showed a defect in responding to auxin in its root development in both white and yellow light conditions, and showed a defect in responding to auxin in hypocotyl elongation in yellow light. Compared to wild type, both shl1-1 and shl2-2 showed increased hypocotyl length in response to cytokinin in white light. Gibberellin (GA) partially recovered shl1-1 mutant phenotype in yellow light, whereas showed no effect on hypocotyl elongation of shl2-2 in this light condition. These altered responses of shl1-1 and shl2-2 to multiple phytohormones in different light regimes suggests that cross-talks among light and hormones regulate SHL1 and SHL2. One of the SHL genes, SHL2 was cloned by map-based positional cloning and shown to be allelic to the previously identified locus designated murus3(mur3) and katamari1(kam1). MUR3/KAM1 encodes a XyG galactosyltransferase. Sequence analysis demonstrated that our original EMS generated reference allele shl2-2 is probably not a null mutant, therefore the phenotypes of T-DNA insertion null mutant in SHL2, SALK_074435 were studied in different light conditions. Unlike shl2-2, SALK_074435 had a slightly short hypocotyl phenotype in the dark (though not to the extent of the det/cop/fus mutants). A consideration of the phenotypes and molecular lesions of shl2-2 and mur3 alleles, along with the phenotypes of null alleles kam1 and SALK_74435, suggests that SHL2/MUR3/KAM1 may be involved in hypocotyl elongation in low light through the modification of xyloglucan in the plant cell wall, and may play a role in hypocotyl elongation in the dark through proper organization of the endomembrane.