Early calcium accumulation may play a role in spongy tissue formation in litchi pericarp

SummaryChanges in the micro-distribution of calcium in litchi (Litchi chinensis Sonn.) pericarp (fruit skin) were studied with an X-ray dispersive spectrometer (electron probe) and the structures of the spongy tissue-forming cells were observed with a transmission electron microscope (TEM) in litchi cvs. 'Huaizhi' (Wai Chee) and 'Nuomici' (No Mai Chee), which differ in cracking susceptibility. Before spongy tissue was visible, calcium had accumulated at the sites of spongy tissue formation, which formed calcium-rich zones in the inner mesocarp. These zones, which included groups of cells, were larger in cracking-resistant 'Huaizhi' than in susceptible 'Nuomici'. 'Huaizhi' pericarp also had a thicker spongy tissue. Cells forming the spongy tissue started to die, with a breakdown of the plasma membrane and tonoplast, plasmolysis, loss of cell contents, swelling and autolysis of the walls. The spongy tissue was initially formed by localized cell death, and later by an increase of intercellular spaces due to the breakdown of middle lamellae. The early accumulation of calcium in spongy tissue-forming cells might have signalled this localized cell death, which falls into the category of programmed cell death (PCD). Calcium-rich zones at the site of spongy tissue formation largely disappeared as spongy tissue was formed, with the endocarp becoming "calcium rich", indicating that intercellular re-localization of calcium may have occurred within the pericarp. The relations between calcium accumulation, spongy tissue formation, and fruit cracking resistance are discussed. We conclude that, in addition to its structural role, calcium also plays a non-structural role in conferring cracking resistance. The accumulation of Ca2+ in early fruit development signals PCD that leads to spongy tissue formation, a process essential for pericarp extension during aril growth.