| The plant cell wall is strong and dynamic, with the ability to loosen and tighten during cell expansion and to become rigid, strong, and resistant to perturbation when full cell expansion has been reached.;Recently, in the last decade, many more techniques to visualize and track cell wall polymer synthesis have been developed, encouraged by the drive to elucidate functions of cell wall components and regulators involved in cell wall synthesis, for the purpose of improving biomass for biofuels.;To this end, as part of a project within the Department of Energy-sponsored Great Lakes Bioenergy Research Center, a collection of over 1,000 Arabidopsis insertional mutant lines with disruptions in cell wall-associated genes and genes encoding receptor-like kinases have been screened for digestibility phenotypes. In this case, digestibility is defined as the yield, measured in terms of percent total dry weight, of glucose and xylose from plant material, after chemical pretreatment and incubation with a commercial enzyme mixture.;There are over 600 receptor-like kinase genes in the model plant Arabidopsis thaliana. Receptor-like kinases have been implicated in various developmental processes such as hormone and small molecule perception in morphological determination and regulation of disease resistance pathways.;To date, only a few dozen receptor-like kinases of Arabidopsis have known functions identified through empirical data. In an attempt to identify the functions of more receptor-like kinases, a reverse-genetics approach was used, employing a collection of mutant Arabidopsis lines with insertions in receptor-like kinase genes. Homozygous insertion lines were challenged with abnormal growth conditions to assay growth and developmental phenotypes. Preliminary data reveals a few putative outliers in hormone responses. One single homozygous recessive mutant displays multi-faceted abnormal growth and developmental phenotype. The abnormal phenotype includes asymmetrical leaf morphology, short stature, and supernumerary axillary branching. The gene disrupted in this mutant encodes a receptor-like cytoplasmic kinase, which does not have an extracellular or transmembrane domain. Molecular rescue of the mutant phenotype restored the wild type phenotype in all aspects of growth and development. |
