Biology subjects

Sokac, A. M.

Publications and source records attributed to Sokac, A. M..

3 recordsLinked to original sources

bioRxiv2025

Cytoplasmic localization of the mRNA encoding actin regulator, Serendipity-α, promotes adherens junction assembly and nuclear repositioning

The subcellular localization of mRNAs is conserved from prokaryotes to humans. In Drosophila embryos [~]70% of mRNAs localize to specific sites in the cytoplasm, but the functional significance of this mRNA localization is largely unknown. During the process of embryo cellularization, mRNA encoding Serendipity- (Sry-), an actin filament (F-actin) binding protein, moves apically, concentrating near centrosomes. Transport is mediated by the Egl/BicD/Dynein complex and requires two stem loops in the 3UTR of the mRNA, which serve as localization signals. mRNA localization is dispensable for Sry- function at cleavage furrows in early cellularization but is necessary for repositioning nuclei in late cellularization. Sry- protein promotes assembly of cortical F-actin and apical spot adherens junctions (AJs) in late cellularization, and these AJs contribute to nuclear repositioning. We suggest that mRNA localization restricts cytoskeletal functions in late cellularization to regulate nuclear repositioning in preparation for the tissue morphogenesis events that immediately follow.

cell biology↗

bioRxiv2025

Drosophila embryo cellularization is modulated by the viscoelastic dynamics of cortical-membrane interactions

1The generation of an epithelial sheet transforms fruit fly embryos from a single syncytial cell directly into a tissue. For this to happen, the apical microvillus membrane is pulled between peripherally anchored nuclei in a process known as furrow invagination. Experimental measurements of furrow invagination velocities have shown that the rate of invagination undergoes slow-to-fast and fast-to-stalled velocity transitions during the formation of individual cells. The causes of such changes are due to multiple intersecting mechanisms and molecular components, including motor proteins, microtubules, and F-actin. In this work, we develop a continuum model to describe the dynamics of furrow invagination. Our model is constrained by previously published experimental data and considers the roles of cytoskeletal forces, cytoplasmic drag, motor protein forces, and membrane tension. We find that the viscous forces produced by the cytoskeleton sliding beneath the plasma membrane dictates furrow velocity. We propose that the slow phase is slow because there is a high density of microvilli, which increases the number of viscous contact points between the plasma membrane and the underlying cytoskeleton. This in turn, results in a higher resistance to furrow invagination. We predict that the fast phase may benefit from fewer cytoskeleton-to-plasma membrane contact points, thus reducing viscous forces and promoting the slow-to-fast switch. Then, we use perturbation and loss-of-function simulations to show that microvillus and sub-apical membrane reservoirs are vital to setting furrow invagination dynamics. This work demonstrates how coupling between the cytoskeleton, the plasma membrane, and distinct membrane reservoirs affects the plasticity and dynamics of cellularization.

cell biology↗

bioRxiv2025

Reducing Cofilin dosage makes embryos resilient to heat stress

In addition to regulating actin dynamics, Cofilin also senses and responds to physiological stress and can determine cell survival outcomes. Yet, the full picture of Cofilin's role in stress response is lacking. Here, we used imaging and RNA-seq methods to show that exposing early Drosophila melanogaster embryos to either acute or chronic heat stress (32{degrees}C) induces a Cofilin-mediated Actin Stress Response (ASR) and leads to upregulation of genes associated with both heat shock and Endoplasmic Reticulum (ER) unfolded protein responses. Reducing cofilin gene dosage (cofilin+/-) in heat-stressed embryos modulates all observed stress responses and partially rescues embryo survival. Unexpectedly we find that heat shock- and ER- stress response modulation arises because non-stressed cofilin+/- embryos already show upregulation of heat shock- and ER- stress response genes, prior to heat exposure. Our data support a model whereby cofilin heterozygosity activates specific stress responses associated with reduced protein homeostasis, thus priming embryos to be more resilient when they encounter subsequent heat stress. We conclude that Cofilin dosage serves as a determinant of stress outcomes, impacting both the actin cytoskeleton and inducible stress response pathways. In the embryo, we identify Cofilin as a novel link between inducible stress response and thermotolerance.

developmental biology↗