<b>βC1 protein</b><b>s promote plant drought tolerance by functionally mimicking an endogenous regulator of</b><b> </b><b>cross-plasma membrane water transport</b>

Plant interactions with biotic factors, such as viruses, often result in altered responses to abiotic stresses like drought. While a handful of case studies are available, the factors and mechanisms underlying these changes remain poorly understood. In this study, we demonstrate that two geminivirus-betasatellite complexes significantly enhance plant survival and the population growth of their insect vectors during water withdrawal. The βC1 protein encoded in betasatellites plays a key role in conferring drought tolerance in an abscisic acid-independent manner. βC1 interacts with the plasma membrane intrinsic protein NbPIP1:1 in Nicotiana benthamiana. In basal conditions, NbPIP1:1 oligomerizes to form water channels, promoting water loss. The water channel activity of NbPIP1:1 is modulated by another aquaporin, NbPIP2:4, which disrupts NbPIP1:1 multimerization and water channel activity by forming hetero-oligomers. Similar to NbPIP2:4, βC1 inhibits NbPIP1:1 multimerization and water channel activity, thereby decreasing water loss and promoting drought tolerance. Our findings uncover a novel molecular mechanism underlying virus-induced drought tolerance, wherein a viral protein mimics the function of an endogenous regulator of cross-plasma membrane water transport.