Body size regulation is affected by different factors in nature, including cell number and cell size. The continued elongation of adult C. elegans, however, involves no changes in cell number and instead relies on cell size. Similar to plants, ploidy is suggested to correlate with the growth of C. elegans, but the main mechanism is unknown. In C. elegans, the Bone Morphogenic Protein (BMP) DBL-1 binds SMA-6 and DAF-4 to activate a signal cascade. This pathway regulates body size and causes changes in hypodermal ploidy that correlate with body size. lon-1 is a downstream component which when mutated produces long worms with increased hypodermal ploidy. Since the function of lon-1 remains unclear, investigative efforts have been directed to examining its genetic interactors for clues into...[ Read more ]

Body size regulation is affected by different factors in nature, including cell number and cell size. The continued elongation of adult C. elegans, however, involves no changes in cell number and instead relies on cell size. Similar to plants, ploidy is suggested to correlate with the growth of C. elegans, but the main mechanism is unknown. In C. elegans, the Bone Morphogenic Protein (BMP) DBL-1 binds SMA-6 and DAF-4 to activate a signal cascade. This pathway regulates body size and causes changes in hypodermal ploidy that correlate with body size. lon-1 is a downstream component which when mutated produces long worms with increased hypodermal ploidy. Since the function of lon-1 remains unclear, investigative efforts have been directed to examining its genetic interactors for clues into its ploidy and body size regulating mechanisms. This study focused on characterising and identifying lon-1 suppressors wx127 and wx132 via genetic mapping, RNAi, Whole Genome Sequencing and complementation tests, and sought to verify whether there is a correlation between body length and ploidy. wx132 was suggested to be dpy-17, and an investigation on dpy genes, extracellular matrix (ECM) components and the regulation of body size and ploidy by lon-1 suggest that lon-1 mutants require an intact cuticular ECM for full elongation. Fluorescent staining of hyp7 nuclei was used to compare ploidy levels between WT and single dpy and ECM component mutants, as well as that between lon-1 mutants and lon-1 double mutants with loss of function dpy or ECM component coding genes. Evidence points to genes encoding ECM being involved in ploidy regulation. In conclusion, lon-1 may regulate body size and ploidy through ECM components, and evidence suggests there is a lack of correlation between body size and ploidy change in C. elegans.