ArticleJournal of experimental botany2021
ALD1 accumulation in Arabidopsis epidermal plastids confers local and non-autonomous disease resistance.
Article in Journal of experimental botany, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
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- Friend or foe: Hybrid proline-rich proteins determine how plants respond to beneficial and pathogenic microbes.Plant physiology · 2022Article
- Emerging Roles of Motile Epidermal Chloroplasts in Plant Immunity.International journal of molecular sciences · 2022Review
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- Genetic requirements for infection-specific responses in conferring disease resistance inFrontiers in plant science · 2022Article
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- A quest for long-distance signals: the epidermis as central regulator of pipecolic acid-associated systemic acquired resistance.Journal of experimental botany · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Arabidopsis plastid-localized ALD1 protein acts in the lysine catabolic pathway that produces infection-induced pipecolic acid (Pip), Pip derivatives, and basal non-Pip metabolite(s). ALD1 is indispensable for disease resistance associated with Pseudomonas syringae infections of naïve plants as well as those previously immunized by a local infection, a phenomenon called systemic acquired resistance (SAR). Pseudomonas syringae is known to associate with mesophyll as well as epidermal cells. To probe the importance of epidermal cells in conferring bacterial disease resistance, we studied plants in which ALD1 was only detectable in the epidermal cells of specific leaves. Local disease resistance and many features of SAR were restored when ALD1 preferentially accumulated in the epidermal plastids at immunization sites. Interestingly, SAR restoration occurred without appreciable accumulation of Pip or known Pip derivatives in secondary distal leaves. Our findings establish that ALD1 has a non-autonomous effect on pathogen growth and defense activation. We propose that ALD1 is sufficient in the epidermis of the immunized leaves to activate SAR, but basal ALD1 and possibly a non-Pip metabolite(s) are also needed at all infection sites to fully suppress bacterial growth. Thus, epidermal plastids that contain ALD1 play a key role in local and whole-plant immune signaling.
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