In C. elegans, TGFb pathway impacts on the body size of the organism in addition to a myriad of other developmental features. The body size of a worm is primarily controlled by endoreduplication that affects the cell size instead of the cell number. Mutants of Lon genes, e.g.,
lon-1,
lon-2 and
lon-3, produce worms 1.5 times longer than wild type. These Lon gene products act in the extracellular matrix regulating the body size, and they encode a PR-related protein, a glypican and a collagen, respectively. Their regulatory mechanism, however, remains unclear. Here, we are particularly interested in
lon-1 and
lon-2 genes which act as negative regulators of the BMP-ligand, DBL-1 in the TGFb pathway. In C, elegans, the effect of LON-1 exerts on DBL-1 was likely through the BMP ligand facilitator, CRM-1, possibly through physical interaction. We mapped the interaction domain between LON-1 and CRM-1 and demonstrated that the LON-1 SCP domain interacts with CR domains on CRM-1. In addition,
lon-2 null mutant allele attributed to two large deletions was characterized. While glypican has the ability to bind BMP ligand, we would investigate this interaction between LON-2 glypican and DBL-1 ligand in vivo. Tagged version of both LON-2 and DBL-1 are expressed in transgenic animals for co-immunoprecipitation and domain mapping. The data from these experiments and the implication will be discussed in this poster. (This study is funded by the Research Grants Council, Hong Kong.).