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Systemic plant signal triggers genome instability
Author(s) -
Filkowski Jody,
Yeoman Allan,
Kovalchuk Olga,
Kovalchuk Igor
Publication year - 2004
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2004.02025.x
Subject(s) - salicylic acid , genome instability , systemic administration , homologous recombination , transgene , radical , recombination , chemistry , rose bengal , endogeny , dna , biology , dna damage , biochemistry , gene , genetics , in vivo
Summary Previously, we have shown that infection of tobacco plants with a viral pathogen triggers local and systemic induction of homologous recombination (HR). Here, we have tested the hypothesis of whether free radicals are potentially involved in the induction of the systemic effect. We report a significant induction of HR in tobacco plants treated with radical‐generating agents, UVC or rose Bengal (RB). Importantly, the recombination increase was observed in local (treated) as well as systemic (non‐treated) tissue. The systemic increase in recombination implies the existence of a signal that is transmitted to non‐treated tissue. Several sets of grafting experiments proved the generation of said signal by both RB and UVC exposure. A statistically significant increase in HR was observed in tissue that received a systemic signal via a grafted leaf. Similar data were obtained from transgenic plants naphthalene degrading salicylate 1‐hydroxylase (NahG) unable to accumulate salicylic acid (SA). Interestingly, pre‐treatment of plants with the radical‐scavenging compound N ‐acetyl‐ l ‐cysteine (NAC) led to a significantly lower recombination increase upon grafting after treatment with UVC and RB. Moreover, leaves taken for grafting from NAC‐pre‐treated plants exhibited a lower level of oxidized organic compounds. Our data suggest the involvement of free radical production in either generation or maintenance of the recombination signal. We discuss potential mechanisms for generation of the signal and possible adaptive advantages of enhanced genomic flexibility following exposure to DNA‐damaging agents.