Award Date

5-15-2026

Degree Type

Thesis

Degree Name

Master of Science (MS)

Department

Life Sciences

First Committee Member

Mo Weng

Second Committee Member

Laurel Raftery

Third Committee Member

Boo Shan Tseng

Fourth Committee Member

Hong Sun

Number of Pages

62

Abstract

Apical constriction is a conserved morphogenetic mechanism that drives epithelial folding during development. During ventral furrow formation in Drosophila melanogaster, contractile actomyosin networks generate forces that reduce apical cell area resulting in tissue invagination. For these cell-scale forces to produce coordinated tissue-scale changes, contractile networks must be mechanically integrated across neighboring cells. Although adherens junctions are known to mediate this coupling, it is unclear how junctions are integrated into cortical actin cytoskeleton, which directly determines cell, and consequently tissue, shape. This thesis tests the hypothesis that supracellular actomyosin organization during apical constriction depends on distinct adherens junction based mechanical couplings: junction-cortical actin network coupling and junction-actomyosin coupling. I further hypothesize that the disruption of these couplings will each result in distinct phenotypes, distinct also from direct weakening of junctions themselves. Identifying these phenotypes will help pinpoint the protein players specifically involved in each coupling mechanism. Fixed and live confocal imaging, and scanning electron microscopy were used to compare phenotypes across conditions using standardized imaging conditions and analysis approaches.

I show that direct weakening of adherens junctions does not cause decoupling of junctions from either actin cortical network or actomyosin filaments until tension forces reach high levels, eventually resulting in irreversible epithelial tearing during ventral furrow formation. By contrast, Diaphanous produced a distinct phenotype consistent with weakened junctioncortical actin network coupling: adherens junctions are detached and displaced from the cell perimeter toward contractile actomyosin at the medial position on the cell apices, resulting in ineffective constriction without tissue tearing. Abelson RNAi produced a similar version of this phenotype. Attempts to test Canoe as a candidate mediator of junction actomyosin coupling using RNAi and germline clone approaches were inconclusive, but these experiments define important future directions for testing the model.

Together, these finding support a model in which junctional actin functions as a mechanical hub that integrates adherens junctions to cortical actin cytoskeleton and therefore enables effective force transmission to promote cell shape changes and tissue changes.

Controlled Subject

Actomyosin; Phenotype; Cells

Disciplines

Biology | Cell Biology | Developmental Biology

File Format

PDF

File Size

1964 KB

Degree Grantor

University of Nevada, Las Vegas

Language

English

Rights

IN COPYRIGHT. For more information about this rights statement, please visit http://rightsstatements.org/vocab/InC/1.0/

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