Refrigerated storage and calcium dips of ripe 'Celeste' sweet cherryfruit: combined effects on cell wall metabolism

Ripening-related firmness loss shortens considerably the storage potential of sweet cherry (Prunus avium L.), thus limiting postharvest handling, transportation, and commercialisation. The biochemical mechanisms underlying this process in cherries are not fully understood, and the mechanisms operati...

Descripción completa

Detalles Bibliográficos
Autores: Belge, Burcu, Goulao, Luis F., Comabella, Eva, Graell i Sarle, Jordi, Lara Ayala, Isabel
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2017
País:España
Institución:Universitat de Lleida (UdL)
Repositorio:Repositori Obert UdL
OAI Identifier:oai:repositori.udl.cat:10459.1/59387
Acceso en línea:https://doi.org/10.1016/j.scienta.2017.02.039
http://hdl.handle.net/10459.1/59387
Access Level:acceso abierto
Palabra clave:Firmness loss
Sweet cherry
Gene expression
Prunus avium L.
Enzims
Fruita de pinyol
Enzymes
Stone fruit
Descripción
Sumario:Ripening-related firmness loss shortens considerably the storage potential of sweet cherry (Prunus avium L.), thus limiting postharvest handling, transportation, and commercialisation. The biochemical mechanisms underlying this process in cherries are not fully understood, and the mechanisms operating in a given fruit may be not extrapolated to a different species. Cell wall materials obtained from untreated and calcium-treated 'Celeste' sweet cherries were fractionated and analysed after cold storage, and related enzyme activities and gene expression were assessed. Calcium-treated fruit were firmer, with lower weight loss and decay incidence than the controls. The accumulation of PaβGal and PaEXP1 transcripts was strongly inhibited in cold-stored fruit, although expression levels recovered largely after three days of shelf life. Data suggest that pectin methylesterase, β-galactosidase and expansin activities may control the access of additional proteins to their substrates. A possible role for the apoplastic redox status in the modulation of the process is also discussed