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Article|01 May 2021|OPEN
Comparative transcriptome analyses shed light on carotenoid production and plastid development in melon fruit
Noam Chayut1,6, Hui Yuan2,3, Yuval Saar1, Yi Zheng4, Tianhu Sun2,3, Xuesong Zhou2,5, Anna Hermanns2,3, Elad Oren1, Adi Faigenboim1, Maixia Hui2, Zhangjun Fei2,4, Michael Mazourek3, Joseph Burger1, Li Li 3,2, & Yaakov Tadmor1,
1Department of Vegetable Research, ARO, Newe Ya’ar Research Center, P. O. Box 1021, Ramat Yishay 30095, Israel
2Robert W. Holley Center for Agriculture and Health, USDA-Agricultural Research Service, Cornell University, Ithaca, NY 14853, USA
3Plant Breeding and Genetics Section, School of Integrative Plant Science, Cornell University, Ithaca, NY 14853, USA
4Boyce Thompson Institute, Ithaca, NY 14853, USA
5State Key Laboratory of Crop Genetics & Germplasm Enhancement, Nanjing Agricultural University, Nanjing 210095, China
6Present address: John Innes Centre, Norwich Research Park, Norwich, UK

Horticulture Research 8,
Article number: 112 (2021)
doi: 10.1038/hortres.2021.112
Views: 282

Received: 15 Oct 2020
Revised: 24 Apr 2021
Accepted: 26 Mar 2021
Published online: 01 May 2021


Carotenoids, such as β-carotene, accumulate in chromoplasts of various fleshy fruits, awarding them with colors, aromas, and nutrients. The Orange (CmOr) gene controls β-carotene accumulation in melon fruit by posttranslationally enhancing carotenogenesis and repressing β-carotene turnover in chromoplasts. Carotenoid isomerase (CRTISO) isomerizes yellow prolycopene into red lycopene, a prerequisite for further metabolism into β-carotene. We comparatively analyzed the developing fruit transcriptomes of orange-colored melon and its two isogenic EMS-induced mutants, low-β (Cmor) and yofi (Cmcrtiso). The Cmor mutation in low-β caused a major transcriptomic change in the mature fruit. In contrast, the Cmcrtiso mutation in yofi significantly changed the transcriptome only in early fruit developmental stages. These findings indicate that melon fruit transcriptome is primarily altered by changes in carotenoid metabolic flux and plastid conversion, but minimally by carotenoid composition in the ripe fruit. Clustering of the differentially expressed genes into functional groups revealed an association between fruit carotenoid metabolic flux with the maintenance of the photosynthetic apparatus in fruit chloroplasts. Moreover, large numbers of thylakoid localized photosynthetic genes were differentially expressed in low-β. CmOR family proteins were found to physically interact with light-harvesting chlorophyll a–b binding proteins, suggesting a new role of CmOR for chloroplast maintenance in melon fruit. This study brings more insights into the cellular and metabolic processes associated with fruit carotenoid accumulation in melon fruit and reveals a new maintenance mechanism of the photosynthetic apparatus for plastid development.