Mutation of the AV2 start codon in SLCCNV impairs viral infectivity under high temperatures, revealing a novel function of viral factors in adaptation to abiotic stress.
Viruses, a group of non-cellular parasites, pose serious threats to human health and agriculture. While viral genetic variations modulating virus adaptation to biotic stresses have been reported, whether and how they affect virus interactions with abiotic stresses such as high temperature remain unknown. Here, we report the impact of AV2 mutations on the life cycle of squash leaf curl China virus (SLCCNV), a bipartite begomoviruses. We first conducted sequence analysis and identified a naturally-occurring mutation at position 35 in AV2 that changes the codon TGG to TAG. Followed analysis revealed that this mutation did not significantly impact SLCCNV infectivity and transmission under both ambient and high temperatures. Next, we changed the start codon of AV2 to stop codon. While the mutation of start codon did not impact SLCCNV infection under ambient temperature, under high temperatures mutant SLCCNV displayed decreased infectivity. We then examined the underpinnings of AV2 function, and found that AV2 cannot compensate for the function of other viral genes and its expression relative to other viral genes was not induced at high temperature. Moreover, protein encoded by AV2 suppressed posttranscriptional gene silencing under both ambient and high temperatures. Our study unravels a novel function of viral factors in the regulation of begomovirus infection under high temperature, and sheds new lights on virus adaptation to abiotic stresses.
Zhang et al. (Wed,) studied this question.