Glufosinate ammonium diminished developments of rice (Oryza sativa) blast and brown leaf spot in 35S:bar-transgenic rice. Pre- and postinoculation treatments of this
herbicide reduced disease development.
Glufosinate ammonium specifically impeded appressorium formation of the pathogens Magnaporthe grisea and Cochliobolus miyabeanus on hydrophobic surface and on transgenic rice. In contrast, conidial germination remained unaffected.
Glufosinate ammonium diminished mycelial growth of two pathogens; however, this inhibitory effect was attenuated in
malnutrition conditions.
Glufosinate ammonium caused slight
chlorosis and diminished
chlorophyll content; however, these alterations were almost completely restored in transgenic rice within 7 d.
Glufosinate ammonium triggered transcriptions of PATHOGENESIS-RELATED (PR) genes and
hydrogen peroxide accumulation in transgenic rice and PR1 transcription in Arabidopsis (Arabidopsis thaliana) wild-type ecotype Columbia harboring 35S:bar construct. All transgenic Arabidopsis showed robust
hydrogen peroxide accumulation by
glufosinate ammonium. This
herbicide also induced PR1 transcription in etr1 and jar1 expressing bar; however, no expression was observed in NahG and npr1.
Fungal infection did not alter transcriptions of PR genes and
hydrogen peroxide accumulation induced by
glufosinate ammonium. Infiltration of
glufosinate ammonium did not affect appressorium formation of M. grisea in vivo but inhibited blast disease development.
Hydrogen peroxide scavengers nullified blast protection and transcriptions of PR genes by
glufosinate ammonium; however, they did not affect brown leaf spot progression. In sum, both direct inhibition of pathogen
infection and activation of defense systems were responsible for disease protection in bar-transgenic rice.