Using a reverse genetic approach, you have identified two mutations in the C. el

Question

Using a reverse genetic approach, you have identified two mutations in the C. elegans dlg-1 gene. dlg-1 encodes a cadherin family member that is critical for proper morphogenesis during worm development — without functional DLG-1 protein, worms fail to gastrulate. For each mutation described below, 1) predict the mechanism by which each mutation prevents gastrulation and 2) draw a simple diagram to contrast how the mutation impacts DLG-1 function relative to wild-type protein.

Your diagram should illustrate a protein-based view that includes the critical components essential to answer the question. Please do not try to diagram a gastrulation defect.

A) a mutation that prevents DLG-1 binding to Ca2+

B) a mutation that leads to a truncated (deleted) cytoplasmic tail

Explanation / Answer

A. DLG-1 is required for the proper formation and function of adherens junctions in C.elegans. Basically DLG-1 is a protein that localized to adherens junctions. In case embryos that lack DLG-1 fail to recruit the proteins to adherens connections. DLG-1 is obligatory for the proper society of the actin cytoskeleton and for the morphological elongation of embryos. The dlg-1/discs large genes are key regulators of epithelial cell polarity in C. elegans and other systems IP(3)/Ca(2+) signaling is involved in the dlg-1 pathway for the establishment of epithelial cell divergence during the development in C. elegans. dlg-1 gene functions during post-embryogenesis and DLG-1 in the polarization of the spermathecal cells. The spermatheca forms an accordion-like organ through which eggs must enter to wide-ranging the ovulation process. Therefore DLG-1-depleted animals exhibit failure of ovulation. In this system consistent with this phenotype apical intersection fails and the PAR-3 protein localized asymmetrically also fails. Such defects suppressed by mutations in inositol polyphosphate 5-phosphatase and in inositol triphosphate receptor, which both are supposed to increase the intracellular Ca(2+) level. Study of embryogenesis exposed that IP(3)/Ca(2+) signaling is also compulsory during junction get-together in embryonic epithelia. So the mutation that prevents DLG-1 binding to Ca2+ prevents the junction get together in embryonic epithelia and effect lots of ovaluation steps and process.

B. The cytoplasmic tail has been shown to be essential for adhesive strengthening and even relatively weak perturbations of adhesion, e.g., by overexpression of wild type cadherins or constructs lacking the cytoplasmic tail, can interfere with the orderly progression of gastrulation. cytoplasmic tail signaling and changes in integrin activation state seems to be regulated by cytoplasmic tail and can regulate a variety of developmentally significant adhesive behaviors. So any mutation incytoplasmic tail would lead to waekended the adhesive strengthening followed by weak perturbations of adhesion.

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