Programmed cell death (PCD) plays a major role in plant development and defense. A fascinating example of developmentally regulated PCD is perforation formation in lace plant (Aponogeton madagascariensis) leaves. Early leaves are furled and have no visible signs of cell death. In newly unfurled leaves cell death starts at the center of each areole and develops towards the veins and stops approximately 4-5 cell layers from the vein. This creates a visible gradient of PCD within an areole composed of three “categories” of cells; non-PCD (NPCD), early-PCD (EPCD), and late-PCD (LPCD). The lace plant is an excellent model system to work on developmentally regulated PCD due to many reasons; the accessibility and predictability of perforation formation, the ability to perform live cell imaging due to the thin and aquatic nature of leaves and established sterile culture system for propagation. Using long term live cell imaging, the order of cellular events and the time course for it were established. Recently, we showed the role of ethylene and vacuolar processing enzymes in lace plant PCD. The first visible sign of lace PCD is the loss of anthocyanin pigmentation. What is the role of anthocyanin/antioxidants in lace PCD? Why does cell death always start at the center? Can we halt the cell death? What triggers cellular death? Why do cells closer to the veins not undergo PCD? Can we induce cell death in these cells? Why do cells display substantial differences to PCD signals? The answers to above questions are currently under investigation in my PCD lab.