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 critcal 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 diagra 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 truncated (deleted) cytoplasmic tail

Explanation / Answer

The protein encoded by the C. elegans discs-large (dlg-1) gene is localised in the zonula adherens and is necessary for correct junctional assembly in all embryonic epithelia. The loss of dlg-1 may affect localisation of additional proteins which are essential for proper differentiation of epithelia in C. elegans. DLG-1 in the zonula adherens depends on the cadherin–catenin system or the basolateral protein LET-413, which is required for the assembly of adherens junctions in C. elegans. The Discs large homolog DLG-1 and its novel binding partner AJM-1 are found in more basal regions of the CeAJ.

dlg-1, a homologue of Drosophila discs large, encodes a MAGUK family scaffolding protein that contains three PDZ domains, one L27 domain, an SH3 domain and a (GuK) guanylate kinase domain. the fragmented junctions of let-413(RNAi) or dlg-1(RNAi) embryos can be partially rescued by depletion of the inositol 5-phosphatase homolog IPP-5. This family of enzymes regulates levels of inositol triphosphate [IP(3)], which can trigger calcium efflux and signaling within the cell. ipp-5 mutants also rescue sterile phenotypes caused by RNAi depletion of PAR-3 in larval stages (which disrupts junction formation in reproductive tract epithelial cells), suggesting that calcium signaling may be a more general regulator of junction formation.

A. A mutation of DLG-1 not binding to Ca+2 will have a severe impact on the signalling events regulating the junction formation. Absence of Ca+2 induced signaling will not trigger the PKC pathway which regulates the junction formation leading to defect in the gastrulation.

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