The impact of ectomycorrhiza formation on monosaccharide transporter gene expression in poplar roots

•  By using degenerate primers, five putative poplar monosaccharide transporter genes were isolated from ectomycorrhizas by RT-PCR. The expression profiles of the three most strongly expressed ones are presented in detail. •  Two transporter genes (PttMST1.2 and PttMST2.2) were down-regulated by ect...

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Veröffentlicht in:The New phytologist. - 1979. - 164(2004), 1 vom: 25. Okt., Seite 147-155
1. Verfasser: Grunze, Nina (VerfasserIn)
Weitere Verfasser: Willmann, Martin, Nehls, Uwe
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2004
Zugriff auf das übergeordnete Werk:The New phytologist
Schlagworte:Journal Article carbohydrate support ectomycorrhiza monosaccharide transporter nutrient demand regulation
Beschreibung
Zusammenfassung:•  By using degenerate primers, five putative poplar monosaccharide transporter genes were isolated from ectomycorrhizas by RT-PCR. The expression profiles of the three most strongly expressed ones are presented in detail. •  Two transporter genes (PttMST1.2 and PttMST2.2) were down-regulated by ectomycorrhiza formation. However, PttMST3.1, which showed 10-times higher expression rates in noninfected roots than any other transporter gene, was up-regulated 12-fold in mycorrhizas. •  While changes in PttMST1.2 and PttMST2.2 expression might be regulated by a fungal metabolite present in axenically grown hyphae, the strong increase of PttMST3.1 expression in mycorrhizas required active plant-fungus interaction. •  Up-regulation of PttMST3.1 by mycorrhiza formation suggests that root cells are able to compete with fungal hyphae for hexoses from the common apoplast during symbiosis, redirecting the sugar-flux back into plant cells whenever the fungal partner does not supply sufficient mineral nutrients. Such a mechanism would enable the plant to link nutrient supply and fungal carbon support at a local level
Beschreibung:Date Revised 20.04.2021
published: Print
GENBANK: AJ698936, AJ698937, AJ698934, AJ698938, AJ698935, AJ407583, AJ407557
Citation Status PubMed-not-MEDLINE
ISSN:1469-8137
DOI:10.1111/j.1469-8137.2004.01158.x