Researchers find key gene in watermelon sweetening

Last updated: 10 Jul, 2020


Edited from a news release (in Chinese).

 

A study by Xu Yong’s research team from the Beijing Academy of Agricultural and Forestry Sciences Vegetable Research Centre has revealed that a new sugar transporter protein, CIVST1, is the key factor in regulating the unloading of sugar from the phloem into watermelon fruit. Revealing the molecular mechanism behind watermelon sweetening provides a new avenue for the selection of high-quality watermelon varieties.

 

Early, wild watermelon was not sweet like the cultivated watermelon of today. Having sweet fruit is not an innate property of watermelons but instead the result of human domestication. Xu Yong’s research team set out to investigate how watermelons become sweet and which genes control these traits.

 

Watermelon fruit. WikiMedia: Shu Suehiro. CC BY 3.0.

 

The sugar produced by photosynthesis in the watermelon leaves is transported to the fruit through sieve elements and companion cell complexes. In earlier studies, Xu Yong’s team revealed that the sugar transporter CITST2 controls the accumulation of sugars in the vacuole, but it remained unclear which transport proteins are involved in the unloading of sugar from the phloem.

 

To identify the sugar transporter, CIVST1, the researchers built an ultra-high density SNP genetic map using 326 watermelon accessions and conducted a map-based cloning and association study. The use of in vitro functional verification and CIVST97 knockout and overexpression lines revealed that CIVST1 is the key factor in regulating sugar unloading in watermelon fruit.

 

The researchers found that CIVST1 was localised to the vacuolar membrane in wild watermelons and localised to the plasma membrane in cultivated watermelons due to a mutation that causes the loss of 45 amino acids at the N-terminal of the protein. They also found that CIVST1 only had sugar transport activity in cultivated watermelons, acting to unload sugar from the phloem tissue. Through genetic analysis of wild and cultivated watermelon accessions with different fruit sugar content, they confirmed that CIVST1 is a domesticated gene. CIVST1 acquired its role in distributing sugar and regulating biological yield during the cultivation of watermelon.

 

Xu Yong’s team have set up a high-sugar, high-quality watermelon molecular breeding program using molecular screening combined with conventional breeding. They have now cultivated the ‘Kingmei’, ‘Jingying’ and other high-quality watermelon varieties with a fruit sugar content as high as 15.7%. ‘The study of sugar transporter genes such as CIVST1 and CITST2 not only establishes the theoretical basis for the accumulation of sugar in watermelon fruits but also provides a rapid molecular identification tool for high-quality watermelon breeding, which will further enhance the level of watermelon breeding in China’ says Xu Yong.

 

Read the paper: Ren, Y., Sun, H., Zong, M., Guo, S., Ren, Z., Zhao, J., Li, M., Zhang, J., Tian, S., Wang, J., Yu, Y., Gong, G., Zhang, H., He, H., Li, L., Zhang, X., Liu, F., Fei, Z. and Xu, Y. (2020) Localization shift of a sugar transporter contributes to phloem unloading in sweet watermelons. New Phytologist. doi: 10.1111/nph.16659