High impact information on RHD3

• These results imply that the RHD3 protein is a member of a new class of GTP-binding proteins that is widespread in eukaryotes and required for regulated cell enlargement [1].
• To define the molecular mechanisms regulating plant cell enlargement, we have conducted a molecular genetic analysis of the ROOT HAIR DEFECTIVE3 (RHD3) gene of Arabidopsis thaliana [1].
• Genetic and physiological analyses suggest that the RHD3 gene is not required for proper cell type specification, and it is likely to act downstream of the hormones auxin and ethylene [1].
• Mutations affecting the RHD3 gene were found to alter cell size, but not cell number, in tissues throughout the plant [1].
• The RHD3 gene was cloned by a T-DNA tagging method and confirmed by the molecular complementation of the rhd3 mutant phenotype and by the analyses of six rhd3 mutant alleles [1].

Biological context of RHD3

• One regulatory region is located between -1,500 and -600 bp upstream of the RHD3 gene and is required for vascular tissue expression [2].
• Consistent with the defective fiber and vessel wall phenotypes, the RHD3 gene exhibited a strong expression in developing fiber and xylem cells [3].
• We showed that the Arabidopsis genome contains two additional RHD3-like genes, one of which was expressed specifically in flowers [3].

Anatomical context of RHD3

• Loss-of-function alleles of ROOT HAIR DEFECTIVE3 (RHD3), a gene previously implicated in the control of vesicle trafficking between the endoplasmic reticulum and the Golgi compartments, resulted in an almost complete suppression of epidermal CFR, root skewing, and waving on hard-agar surfaces [4].
• Using this assay for quantitative sublethal perturbation of secGFP transport, we identify a role for root hair defective 3 (RHD3) in transport of secreted and Golgi markers between the ER and the Golgi apparatus [5].
• The yeast SEY1 is a homolog of the Arabidopsis RHD3 gene whose mutations cause the accumulation of transport vesicles near the tips of defective root hairs [6].
• Our findings suggest an essential role of RHD3 in cell wall biosynthesis and actin organization, both of which are known to be important for cell expansion [3].
• In addition, we found that mutation of the RHD3 gene caused an alteration in the organization of the actin cytoskeleton but no effects on cortical microtubules [3].

Associations of RHD3 with chemical compounds

• Analyses with a secretion inhibitor, Brefeldin A, and with an rhd3 mutant defective in the secretion process in root epidermis suggested that intercellular CPC movement is mediated through plasmodesmata [7].

Other interactions of RHD3

• For example, we show that TIP1 and RHD3 are required much earlier in hair formation than previous studies have suggested [8].
• The COW1 locus of arabidopsis acts after RHD2, and in parallel with RHD3 and TIP1, to determine the shape, rate of elongation, and number of root hairs produced from each site of hair formation [9].

Analytical, diagnostic and therapeutic context of RHD3

• To obtain insight into the mechanisms of RHD3 regulation, we conducted a molecular genetic dissection of RHD3 gene expression and function [2].
• To demonstrate that the libraries contained high quality longer cDNAs, a fragment located 2.7 kb from the 3' end of the cDNA of the single copy root-hair expressed gene RHD3 was cloned using a nested PCR strategy [10].

References