Restraining Quiescence Release-Related Ageing in Plant Cells: A Case Study in Carrot

Author:

Schulz Katie1ORCID,Machaj Gabriela2ORCID,Knox Paul1,Hancock Robert D.3ORCID,Verrall Susan R.4,Korpinen Risto5ORCID,Saranpää Pekka5,Kärkönen Anna5,Karpinska Barbara6,Foyer Christine H.6ORCID

Affiliation:

1. Centre for Plant Sciences, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK

2. Department of Plant Biology and Biotechnology, University of Agriculture in Krakow, 31-120 Krakow, Poland

3. Cell and Molecular Sciences, The James Hutton Institute, Invergowrie, Dundee DD2 5DA, UK

4. Ecological Sciences, The James Hutton Institute, Invergowrie, Dundee DD2 1BE, UK

5. Natural Resources Institute Finland, Production Systems, Latokartanonkaari 9, 00790 Helsinki, Finland

6. School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston B15 2TT, UK

Abstract

The blackening of cut carrots causes substantial economic losses to the food industry. Blackening was not observed in carrots that had been stored underground for less than a year, but the susceptibility to blackening increased with the age of the carrots that were stored underground for longer periods. Samples of black, border, and orange tissues from processed carrot batons and slices, prepared under industry standard conditions, were analyzed to identify the molecular and metabolic mechanisms underpinning processing-induced blackening. The black tissues showed substantial molecular and metabolic rewiring and large changes in the cell wall structure, with a decreased abundance of xyloglucan, pectins (homogalacturonan, rhamnogalacturonan-I, galactan and arabinan), and higher levels of lignin and other phenolic compounds when compared to orange tissues. Metabolite profiling analysis showed that there was a major shift from primary to secondary metabolism in the black tissues, which were depleted in sugars, amino acids, and tricarboxylic acid (TCA) cycle intermediates but were rich in phenolic compounds. These findings suggest that processing triggers a release from quiescence. Transcripts encoding proteins associated with secondary metabolism were less abundant in the black tissues, but there were no increases in transcripts associated with oxidative stress responses, programmed cell death, or senescence. We conclude that restraining quiescence release alters cell wall metabolism and composition, particularly regarding pectin composition, in a manner that increases susceptibility to blackening upon processing.

Funder

UKRI

Publisher

MDPI AG

Subject

General Medicine

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