Flower longevity, one of the most important characteristics of horticulture crops, is determined by the senescence of petals. However, the regulatory mechanisms involved in petal senescence remain elusive. Autophagy, a pathway that is widely studied for longevity, plays an important role in the regulation of petal senescence. Previous research and our preliminary results show that the expression of two central autophagy genes, Autophagy Gene 6 (ATG6) and Phosphoinositide 3-kinase (PI3K), increases during petal senescence. We hypothesized that suppressing autophagy gene expression would decrease flower longevity. To characterize the role of ATG6 and PI3K in petal senescence, we used Virus-Induced Gene Silencing (VIGS) to suppress individual genes in Petunia ï‚´ hybrida. Our results showed that the expression of ATG6 and PI3K was down-regulated and it resulted in early petal senescence, reduced flower numbers, and lower flower and shoot dry weight in petunia. We also found no difference in virus levels in plants in the VIGS experiments. Interestingly, our experiment showed a type I metacaspase gene MC1, another important regulator of senescence from the apoptosis pathway in plants, was suppressed in the ATG6- and PI3K-silenced plants, indicating an interaction between autophagy and apoptosis. Based on these results, we conclude that ATG6 and PI3K are negative regulators of petal senescence and are critical for other important flower features. Petal senescence is regulated by a complex network of metabolic pathways. The results of this project will be fundamental for future studies of petal senescence and will provide genetic information for crop improvement.