Change in RhoGAP and RhoGEF availability drives transitions in cortical patterning and excitability in Drosophila.

Area of Science:

• Cell Biology
• Developmental Biology
• Biochemistry

Background:

• Actin cortex dynamics are vital for cell shape changes and collective cell behaviors during development.
• Mechanisms governing developmental transitions in vivo remain poorly understood, particularly regarding specific molecular regulators.

Purpose of the Study:

• To identify molecular mechanisms and conditions that regulate actin cortex patterning and dynamics during Drosophila development.
• To elucidate the roles of specific RhoGEF and RhoGAP proteins in actomyosin wave formation.

Main Methods:

• Utilized two developmental systems in Drosophila melanogaster.
• Investigated the effects of depleting or overexpressing specific RhoGEF and RhoGAP proteins (Ect2, RhoGAP15B, RhoGEF2, C-GAP).
• Analyzed protein localization, actomyosin wave induction, RhoA activation, and F-actin dynamics.

Main Results:

• Identified a RhoGEF (Ect2) and RhoGAP (RhoGAP15B) pair essential for actomyosin waves in egg chambers; their depletion disrupted wave induction.
• Showed that RhoGEF2 and C-GAP overexpression induced actomyosin waves in early embryos, with RhoA activation preceding actomyosin assembly.
• Demonstrated that F-actin dynamics influence RhoA signaling and cytoskeletal organization within waves, affecting wave period and width.

Conclusions:

• A specific RhoGEF/RhoGAP pair mechanism is crucial for inducing actomyosin waves, essential for oocyte development.
• This mechanism is conserved and applicable to other cell types, including epithelial and syncytial cells.
• F-actin dynamics may play a role in negative feedback regulation of actomyosin waves.