Proteome impact on maize silks under the priming state induced by Trichoderma root colonization
Main conclusion Trichoderma activates plant proteins to counteract Fusarium infection. Comparison between proteomic and transcriptomic data suggests differential response regulation. Proteins from the phenylpropanoid pathway are activated to quickly respond to pathogen attack. Trichoderma species ca...
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Veröffentlicht in: | Planta 2021-05, Vol.253 (5), p.115-115, Article 115 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Main conclusion
Trichoderma
activates plant proteins to counteract
Fusarium
infection. Comparison between proteomic and transcriptomic data suggests differential response regulation. Proteins from the phenylpropanoid pathway are activated to quickly respond to pathogen attack.
Trichoderma
species can stimulate local and distant immune responses in colonized plant tissues to prevent future pathogenic attacks. Priming of plant defenses is characterized by changes in transcriptional, metabolic, and epigenetic states after stimulus perception. We have previously investigated transcriptional reprogramming in silk tissues from maize plants inoculated with
Trichoderma atroviride
and challenged with
Fusarium verticillioides
(Agostini et al., Mol Plant-Microbe In 32:95–106, 2019). To better understand the molecular changes induced by
T. atroviride
in maize, a proteomic approach was conducted in this instance. Several proteins belonging to different metabolic categories were detected as priming-involved proteins. However, we detected a very low correlation with those priming-modulated transcripts suggesting the importance of regulatory events a posteriori of the transcriptional process to accomplish the final goal of blocking pathogen entry. Specifically, we focused on the phenylpropanoid pathway, since we detected several proteins that are upregulated in the priming state and might explain cell wall reinforcement as well as the increase in flavonoid and lignin content in maize silks after activation of induced systemic resistance. |
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ISSN: | 0032-0935 1432-2048 |
DOI: | 10.1007/s00425-021-03633-0 |