Articles
The progression of programmed cell death hallmarks in low oxygen-treated ‘Conference’ pear tissue
Article number
1396_7
Pages
47 – 52
Language
English
Abstract
Pear fruit (Pyrus × communis Conference) is one of the most valuable commercial crops in Belgium.
Since fruits continue important metabolic processes like respiration, postharvest storage conditions aim to extend shelf-life through low temperatures, hypoxic conditions, and slightly elevated carbon dioxide.
Unfortunately, disorders including internal browning and cavity formation are commonly induced, indicating a type of local cell death.
However, limited understanding of the molecular regulation behind postharvest disorder development in pear fruit remains a major challenge.
It is hypothesized that this process is controlled through the process of programmed cell death (PCD). To verify the potential role of PCD in the pore and cavity formation in pear fruit during postharvest storage, Conference pear tissue slices were subjected to different hypoxic conditions (21 kPa O2 as control, 3, 0.5, and 0 kPa O2) and sampled over a 72-h period.
A set of PCD hallmarks or cellular features indicating that PCD has been initiated or completed, were tracked throughout the experiment.
Testing membrane permeabilization by Evans blue staining showed 21 and 0.5 kPa O2-treated tissue to have the greatest dye uptake, followed by N2-treated tissue.
Nuclear changes and DNA fragmentation, detected by DAPI (4,6-diamidino-2-phenylindole) and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assays, respectively, indicated a significant difference in the cell death rate of all treatments versus 3 kPa O2-treated tissue.
These early signs of PCD in response to low oxygen stress were observed prior any visual pore formation.
Transcriptomic analyses of PCD-related genes is ongoing to resolve the molecular events underpinning the different treatments.
In future work, pear fruits during long-term storage will also be characterized in relation to oxygen gradients present in bulky fruit.
Since fruits continue important metabolic processes like respiration, postharvest storage conditions aim to extend shelf-life through low temperatures, hypoxic conditions, and slightly elevated carbon dioxide.
Unfortunately, disorders including internal browning and cavity formation are commonly induced, indicating a type of local cell death.
However, limited understanding of the molecular regulation behind postharvest disorder development in pear fruit remains a major challenge.
It is hypothesized that this process is controlled through the process of programmed cell death (PCD). To verify the potential role of PCD in the pore and cavity formation in pear fruit during postharvest storage, Conference pear tissue slices were subjected to different hypoxic conditions (21 kPa O2 as control, 3, 0.5, and 0 kPa O2) and sampled over a 72-h period.
A set of PCD hallmarks or cellular features indicating that PCD has been initiated or completed, were tracked throughout the experiment.
Testing membrane permeabilization by Evans blue staining showed 21 and 0.5 kPa O2-treated tissue to have the greatest dye uptake, followed by N2-treated tissue.
Nuclear changes and DNA fragmentation, detected by DAPI (4,6-diamidino-2-phenylindole) and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assays, respectively, indicated a significant difference in the cell death rate of all treatments versus 3 kPa O2-treated tissue.
These early signs of PCD in response to low oxygen stress were observed prior any visual pore formation.
Transcriptomic analyses of PCD-related genes is ongoing to resolve the molecular events underpinning the different treatments.
In future work, pear fruits during long-term storage will also be characterized in relation to oxygen gradients present in bulky fruit.
Authors
A.J. Ty, M. Hertog, B. Nicolaï
Keywords
programmed cell death, pear, low oxygen stress, hypoxia, tissue browning
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