All Publications

  • Imaginal disk growth factors are Drosophila chitinase-like proteins with roles in morphogenesis and CO2 response GENETICS Sustar, A. E., Strand, L. G., Zimmerman, S. G., Berg, C. A. 2022


    Chitinase-like proteins (CLPs) are members of the family 18 glycosyl hydrolases, which include chitinases and the enzymatically inactive CLPs. A mutation in the enzyme's catalytic site, conserved in vertebrates and invertebrates, allowed CLPs to evolve independently with functions that do not require chitinase activity. CLPs normally function during inflammatory responses, wound healing, and host defense, but when they persist at excessive levels at sites of chronic inflammation and in tissue-remodeling disorders, they correlate positively with disease progression and poor prognosis. Little is known, however, about their physiological function. Drosophila melanogaster has six CLPS, termed Imaginal disc growth factors (Idgfs), encoded by Idgf1, Idgf2, Idgf3, Idgf4, Idgf5, and Idgf6. In this study we developed tools to facilitate characterization of the physiological roles of the Idgfs by deleting each of the Idgf genes using the CRISPR/Cas9 system and assessing loss-of-function phenotypes. Using null lines, we showed that loss-of-function for all six Idgf proteins significantly lowers viability and fertility. We also showed that Idgfs play roles in epithelial morphogenesis, maintaining proper epithelial architecture and cell shape, regulating E-cadherin and cortical Actin, and remarkably, protecting these tissues against CO2 exposure. Defining the normal molecular mechanisms of CLPS is key to understanding how deviations tip the balance from a physiological to a pathological state.

    View details for DOI 10.1093/genetics/iyac185

    View details for Web of Science ID 000912772800001

    View details for PubMedID 36576887

  • A new partial loss of function allele of rad-54.L. microPublication biology Akerib, C. C., Yokoo, R., Nsamba, E. T., Strand, L. G., Yamaya, K., Villeneuve, A. M. 2022; 2022


    RAD-54.L is required for the repair of meiotic double-strand DNA breaks (DSBs), playing an essential role in promoting removal of recombinase RAD-51 and normal completion of meiotic recombination. Failure to complete meiotic DSB repair leads to 100% lethality of embryos produced by rad-54.L null mutant mothers. Here we report a new partial loss of function allele, rad-54.L(me139) , that may prove useful for investigating meiotic mechanisms by providing a sensitized genetic background that reduces but does not eliminate the essential functions of RAD-54.L.

    View details for DOI 10.17912/micropub.biology.000637

    View details for PubMedID 36247323