Virus innexin expression in insect cells disrupts cell membrane potential and pH

Area of Science:

• Virology
• Insect Pathology
• Molecular Biology

Background:

• Parasitoid wasps utilize Polydnaviruses, encoding virulence factors, for caterpillar parasitization.
• Ichnoviruses, a Polydnavirus group, possess Vinnexins, homologous to insect gap junction genes, which may influence host cell physiology.

Purpose of the Study:

• Investigate the role of Vinnexins in host pathology.
• Elucidate the mechanism by which Vinnexins affect caterpillar host cell physiology.

Main Methods:

• Generated recombinant baculoviruses to express Vinnexins in Spodoptera frugiperda (Sf9) cells.
• Assessed cell physiological changes using membrane potential-sensitive (DiBac4(3)) and pH (CFDA) probes.
• Utilized carbenoxolone and ouabain to investigate the roles of gap junctions, hemi-channels, and Na+/K+-ATPase.

Main Results:

• Vinnexins induced specific cell membrane depolarization and cytoplasmic alkalization in Sf9 cells.
• Neither Vinnexin hemi-channels nor Na+/K+-ATPase directly explained these observed effects.
• Individual Vinnexin proteins demonstrated differential effects on host cell physiology.

Conclusions:

• Vinnexin proteins may disrupt host cell physiology by altering bio-electrical phenomena.
• The Vinnexin protein family exhibits distinct impacts on host physiology, suggesting specific roles in parasitization.