The control of the body sizes of organisms has long been a topic of interest in developmental biology. In the past decade, Caenorhabditis elegans (C. elegans) has been used to reveal the principles that underlie the control of body size. Well-characterized developmental processes of C. elegans facilitate in-depth investigations of the growth regulation that involves many genes. Bone morphogenetic protein (BMP) pathways, a sub-family of the transforming growth factor (TGF)-beta signaling pathways, is one of the major regulatory pathways that control the C. elegans body length. The BMP signal is activated by the binding of DBL-1 to the receptors, transduced to the nucleus of the cell by Smad proteins. The transcription of target genes is regulated by the BMP signal strength, and thus cont...[ Read more ]

The control of the body sizes of organisms has long been a topic of interest in developmental biology. In the past decade, Caenorhabditis elegans (C. elegans) has been used to reveal the principles that underlie the control of body size. Well-characterized developmental processes of C. elegans facilitate in-depth investigations of the growth regulation that involves many genes. Bone morphogenetic protein (BMP) pathways, a sub-family of the transforming growth factor (TGF)-beta signaling pathways, is one of the major regulatory pathways that control the C. elegans body length. The BMP signal is activated by the binding of DBL-1 to the receptors, transduced to the nucleus of the cell by Smad proteins. The transcription of target genes is regulated by the BMP signal strength, and thus controls the animal growth. Recently, a BMP facilitator, CRM-1, has been found to have putative physical interaction with the product of a target gene of a BMP pathway, LON-1. This observation confers the possibility that LON-1 could regulate the BMP signaling event via physical interaction with CRM-1.

In this study, the CRM-1;LON-1 physical interaction is tested and the interaction domains are mapped by a yeast-2-hybrid assay. The SCP-domain on LON-1 and the cysteine-rich (CR) domain on CRM-1 are responsible for this interaction. Moreover, the establishment of a genetic relationship between crm-1 and lon-1 is attempted, yet no clear cut epistatic relationship can be revealed as the crm-1;lon-1 double mutant displays an intermediate phenotype. The molecular function of LON-1 is investigated, and a dominant negative effect cannot be observed by the ectopic expression of lon-1 complementary DNA (cDNA) in the GABA neurons and body wall muscle in wild-type (WT) animals. The results suggest that lon-1 can only perform its function at the hypodermis. Finally, transcriptional reporter lon-1::gfp is generated to investigate the effect of mutations in crm-1 and lon-1. The possible self-regulation of lon-1 by a negative feedback mechanism is revealed and then discussed.