# A bacterial effector protein targets plant ferredoxin-NADP+ reductase to promote infection

## TL;DR

A bacterial protein from Ralstonia solanacearum disrupts plant energy production to weaken defenses and promote infection.

## Contribution

Discovery of a bacterial effector protein that targets plant ATP production to enhance pathogenicity.

## Key findings

- RipAF1 interacts with plant FNR, reducing ATP levels and suppressing immunity.
- Exogenous ATP application increases plant resistance to R. solanacearum.
- ATP plays a key role in plant defense against this bacterial pathogen.

## Abstract

Pathogenic bacteria utilize a type III secretion system to translocate effector proteins into plant cells, where they inhibit plant immunity or interfere with normal cellular functions to facilitate infection. Whether and how pathogen effectors manipulate plant adenosine 5’-triphosphate (ATP) to facilitate infection remains largely unknown. In this work, we show that an effector protein, RipAF1, from the plant pathogen Ralstonia solanacearum suppresses flg22-induced immune activation and contributes to virulence. RipAF1 physically interacts with plant ferredoxin-NADP+ reductase (FNR), which is involved in NADPH and ATP production, in chloroplast. Transient expression of FNR leads to increased ATP accumulation and resistance against R. solanacearum, while co-expression of FNR with RipAF1 significantly reduced ATP levels. We further show that exogenous application of ATP enhances plant resistance to R. solanacearum infection. Our findings indicate a key role of ATP in plant resistance against R. solanacearum, and elucidate a bacterial virulence strategy wherein pathogenicity is enhanced through targeted modification of host ATP homeostasis via bacterial effector proteins.

Immune responses are highly energy-consuming processes. ATP, the universal energy currency for cellular processes, is essential for the immune responses that plants and animals need to defend against pathogen attacks. Extracellular ATP can also function as damage-associated molecular pattern to trigger defense reaction. Type III secretion systems and their secreted effector proteins are key virulence factors for bacterial pathogens. These effector proteins have long been thought to primarily directly suppress host immunity. However, emerging evidence indicates that pathogen effector proteins can also interfere with other cellular processes, such as hormone metabolism and protein degradation, to indirectly inhibit plant immunity.

In this study, we discovered that RipAF1, an effector protein from the broad-host plant pathogen Ralstonia solanacearum, interacts with ferredoxin-NADP⁺ reductase (FNR) in the host. FNR is a flavoenzyme involved in ATP production, and RipAF1 can reduce the host’s ATP content. Furthermore, we demonstrated that ATP pre-treatment can enhance plant resistance to R. solanacearum infection. Our research not only reveals the positive role of ATP in plant defense against this bacterial pathogen but also proposes a new molecular mechanism by which pathogens promote infection through interference with host energy metabolism.