Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/74251
Title: Methyl salicylate retards mitochondria-mediated programmed cell death in peel spotting of ‘Sucrier’ banana during storage
Authors: Sirawich Chotikakham
Aussara Panya
Kobkiat Saengnil
Authors: Sirawich Chotikakham
Aussara Panya
Kobkiat Saengnil
Keywords: Agricultural and Biological Sciences
Issue Date: 1-Dec-2022
Abstract: Programmed cell death (PCD) has recently come forth as an important mechanism for plant development and been associated with the response to abiotic and biotic stresses, disease-induced abnormal development and disorders. The objective of this study was to investigate the effect of methyl salicylate (MeSA) treatment in relation to PCD during the natural development of peel spotting of ‘Sucrier’ banana. During the storage, the ripen fruit were examined morphologically and biochemically. The results suggested a connection between PCD and peel spotting development. Prominent PCD markers, such as caspase-like activity, DNA degradation and cell death were increasingly noticeable along with the severity of spotting lesion. MeSA treatment activated the expression of anti-apoptotic genes; BI1, BAG1 and 14–3–3ι. The enhanced expression of these genes gave rise to lowering of caspase 8, 9 and 3-like activities and DNA degradation. The reduction in the caspase-like activity corresponded well with the reduction of late PCD markers such as DNase activity and poly (ADP-ribose) polymerase cleavage and propidium iodide uptake. Our study reveals a potential role of PCD in peel spotting development and how MeSA intervenes the process. The findings suggested that MeSA upregulates the expression of anti-apoptotic genes which, in turn, play a key role in retarding mitochondria-mediated PCD activation, thereby mitigating the peel spotting of ‘Sucrier’ banana.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85137693891&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/74251
ISSN: 09255214
Appears in Collections:CMUL: Journal Articles

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