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Metabolomics of tomato xylem sap during bacterial wilt reveals Ralstonia solanacearum produces abundant putrescine, a metabolite that accelerates wilt disease
Author(s) -
LowePower Tiffany M.,
Hendrich Connor G.,
von RoepenackLahaye Edda,
Li Bin,
Wu Dousheng,
Mitra Raka,
Dalsing Beth L.,
Ricca Patrizia,
Naidoo Jacinth,
Cook David,
Jancewicz Amy,
Masson Patrick,
Thomma Bart,
Lahaye Thomas,
Michael Anthony J.,
Allen Caitilyn
Publication year - 2018
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.14020
Subject(s) - ralstonia solanacearum , bacterial wilt , xylem , biology , putrescine , wilt disease , botany , microbiology and biotechnology , pathogen , biochemistry , enzyme
Summary Ralstonia solanacearum thrives in plant xylem vessels and causes bacterial wilt disease despite the low nutrient content of xylem sap. We found that R. solanacearum manipulates its host to increase nutrients in tomato xylem sap, enabling it to grow better in sap from infected plants than in sap from healthy plants. Untargeted GC/MS metabolomics identified 22 metabolites enriched in R. solanacearum ‐infected sap. Eight of these could serve as sole carbon or nitrogen sources for R. solanacearum . Putrescine, a polyamine that is not a sole carbon or nitrogen source for R. solanacearum , was enriched 76‐fold to 37 µM in R. solanacearum ‐infected sap. R. solanacearum synthesized putrescine via a SpeC ornithine decarboxylase. A Δ speC mutant required ≥ 15 µM exogenous putrescine to grow and could not grow alone in xylem even when plants were treated with putrescine. However, co‐inoculation with wildtype rescued ΔspeC growth, indicating R. solanacearum produced and exported putrescine to xylem sap. Intriguingly, treating plants with putrescine before inoculation accelerated wilt symptom development and R. solanacearum growth and systemic spread. Xylem putrescine concentration was unchanged in putrescine‐treated plants, so the exogenous putrescine likely accelerated disease indirectly by affecting host physiology. These results indicate that putrescine is a pathogen‐produced virulence metabolite.