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The Role of Sugar Transporter Genes during Early Infection by Root-Knot Nematodes

Although pathogens such as nematodes are known to hijack nutrients from host plants, the mechanisms whereby nematodes obtain sugars from plants remain largely unknown. To determine the effects of nematode infection on host plant sugar allocation, soluble sugar (fructose, glucose, sucrose) content wa...

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Detalles Bibliográficos
Autores principales: Zhao, Dan, You, Yang, Fan, Haiyan, Zhu, Xiaofeng, Wang, Yuanyuan, Duan, Yuxi, Xuan, Yuanhu, Chen, Lijie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5796247/
https://www.ncbi.nlm.nih.gov/pubmed/29351253
http://dx.doi.org/10.3390/ijms19010302
Descripción
Sumario:Although pathogens such as nematodes are known to hijack nutrients from host plants, the mechanisms whereby nematodes obtain sugars from plants remain largely unknown. To determine the effects of nematode infection on host plant sugar allocation, soluble sugar (fructose, glucose, sucrose) content was investigated using high-performance liquid chromatography with refractive index detection and was found to increase significantly in tomato (Solanum lycopersicum, Sl) leaves and roots during early infection by root-knot nematodes (RKNs). To further analyze whether sugar transporters played a role in this process, the expression levels of sucrose transporter (SUT/SUC), Sugars Will Eventually be Exported Transporter (SWEET), tonoplast monosaccharide transporter (TMT), and vacuolar glucose transporter (VGT) gene family members were examined by qRT-PCR analysis after RKN infection. The results showed that three SlSUTs, 17 SlSWEETs, three SlTMTs, and SlVGT1 were upregulated in the leaves, whereas three SlSUTs, 17 SlSWEETs, two SlTMTs, and SlVGT1 were induced in the roots. To determine the function of the sugar transporters in the RKN infection process, we examined post-infection responses in the Atsuc2 mutant and pAtSUC2-GUS lines. β-glucuronidase expression was strongly induced at the infection sites, and RKN development was significantly arrested in the Atsuc2 mutant. Taken together, our analyses provide useful information for understanding the sugar transporter responses during early infection by RKNs in tomato.