MITOCHONDRIAL SMALL HEAT SHOCK PROTEIN AND CHILLING TOLERANCE IN TOMATO FRUIT

MARIELA ESCOBAR; IVO FEUSSNER; HERRFURTH CORNELIA; ESTELA VALLE; SILVANA BOGGIO

Salta

Congreso; LV Annual SAIB Meeting and XIV PABMB Congress; 2019

SAIB

Chilling injury (CI) is a physiological disorder that appears when plants and plant organs are exposed to low, but non-freezing temperatures. In tomato fruit, low temperature is used as a strategy to extend the commercialization period after harvesting. But this procedure can lead to CI affecting the production yield and quality. A comparative study showed contrasting postharvest chilling tolerance between two tomato varieties, cv. Micro-Tom was more tolerant while cv. Minitomato showed susceptibility to CI. It was previously reported that these two varieties exhibited different expression of small Heat Shock Proteins (sHSPs) after chilling, with an increase of sHSPs in Micro-Tom while the more susceptible Minitomato fruit showed down-regulation of all sHSPs analyzed during cold storage. Among them, one mitochondrial sHSPs (sHSP23.8) showed higher expression in Micro-Tom green mature fruit after cold storage indicating a potential correlation between the accumulation of sHSP23.8 and the amelioration of chilling symptoms in tomato fruit. Considering that tomato has only one mitochondria-located sHSP, the functional consequences of the down-regulation of sHSP23.8 in tomato fruit was investigated by using knockdown mutants. Knockdown fruit of sHSP23.8 were analyzed in their phenotype and susceptibility to CI directly after and during several days after chilling treatments. Symptoms of CI were especially evident in amiR23.8 fruit after 15 days of recovery. Compared to WT, amiR23.8 fruit showed partial discoloration, wilting and wrinkles at the surface. In addition, pre-chilled fruit of amiR23.8 mutant showed higher loss of water and increased ion leakage of pericarp tissue compared to WT fruit. The amiR23.8 fruit deterioration indicates that it is highly susceptible to cold stress and developed chilling injury symptoms. The lipidome of fruit after chilling of amiR23.8 showed altered amounts of glycerolipids, and the level of saturated lipids in amiR23.8 decreased, but not lower than the level in WT under normal conditions. The opposite was found in the relative percentage of unsaturated lipids, having amiR23.8 fruit significantly lower levels in normal conditions and after chilling. The results indicate a differential degradation of extraplastidic and plastidic lipids in amiR23.8 fruit, and alterations in the remodeling of the lipidome after cold stress, which may lead to higher sensitivity to chilling injury. The results presented here suggest that sHSP23.8 may be directly involved in the protection mechanisms against chilling stress in tomato fruit.