Abstract: elongation defective (eld1), a recessive gamma ray induced mutation in Arabidopsis, was reported to affect cell growth and differentiation, resulting in a mutant with a diminutive stature and pleiotropic phenotypes. Since cell growth is the primary defect in the mutant, it was hypothesized that the primary function of ELD1 is to promote cell growth. Defect in cell growth affected the subsequent differentiation. Here I present an extensive analysis of the ELD1 gene. Using the map-based positional cloning approach, I cloned ELD1 and found that it is located on the upper arm of chromosome 3 and encodes a novel serine-rich protein. I analyzed the ELD1 homologous genes and found that it belongs to a new family of plant-specific protein that has a novel molecular function. I also studied the expression level and pattern of ELD1 and showed that it is expressed ubiquitously in every organ at a low level. Using reverse genetics, I also identified additional eld1 allele, eld1-2, and characterized its phenotype. I constructed double mutants to investigate the relationship of ELD1 with other Arabidopsis genes that were known to regulate growth. Having characterized the structure and function of the ELD1 gene, I focused on analyzing the subcellular location of the ELD1 protein. Using GREEN FLUORESCENT PROTEIN reporter protein fused to ELD1, I showed that ELD1 is localized to the cell wall/extracellular space. I also studied the function of the N-terminal sequence of ELD1 and demonstrated that the sequence can direct ELD1 to the cell wall/extracellular space. I discussed this result in relation to the results presented by two other laboratories that independently identified ELD1 as KOBITO1 (KOB1) and ABSCISIC ACID-INSENSITIVE 8 (ABI8). Additionally, I described my attempt to identify the ELD1 interacting proteins and to detect the ELD1-GFP fusion proteins in the transgenic plants using western blot and genetic approach. Finally, I studied the responses of eld1 to sugars and abscisic acid and showed that unlike the allele of abi8 reported, eld1 does not have a defect in the response to these substances. Results from these studies support the original hypothesis that the primary function of ELD1 is to promote cell growth. The mode of its action is likely through acting as the cell wall, supporting the growing cell as it elongates or by acting as a diffusible signaling protein.