Sinorhizobium fredii HH103 nolR and nodD2 mutants gain capacity for infection thread invasion of Lotus japonicus Gifu and Lotus burttii
2019
Sinorhizobium frediiHH103 Rifᴿ, a broad‐host‐range rhizobial strain, forms ineffective nodules with
Lotus japonicusbut induces nitrogen‐fixing nodules in
Lotusburttii roots that are infected by intercellular entry. Here we show that HH103 Rifᴿ nolR or nodD2 mutants gain the ability to induce infection thread formation and to form nitrogen‐fixing nodules in L. japonicus Gifu. Microscopy studies showed that the mode of infection of L. burttii roots by the nodD2 and nolR mutants switched from intercellular entry to infection threads (ITs). In the presence of the
isoflavone
genistein, both mutants overproduced
Nod‐factors. Transcriptomic analyses showed that, in the presence of
Lotus japonicusGifu root exudates, genes related to
Nod factorsproduction were overexpressed in both mutants in comparison to HH103 Rifᴿ. Complementation of the nodD2 and nolR mutants provoked a decrease in
Nod‐factorproduction, the incapacity to form nitrogen‐fixing nodules with L. japonicus Gifu and restored the intercellular way of infection in L. burttii. Thus, the capacity of S. fredii HH103 Rifᴿ nodD2 and nolR mutants to infect L. burttii and L. japonicus Gifu by ITs and fix nitrogen L. japonicus Gifu might be correlated with
Nod‐factor
overproduction, although other bacterial symbiotic signals could also be involved.
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