Modulation of Anaphase‐Promoting Complex Genes Regulates Root‐Knot Nematode Gall Development and Plant Susceptibility
4 affiliations
- 1INRAE Université Côte d'Azur, CNRS Sophia Antipolis France
- 2Laboratório de Biologia Molecular de Plantas, Instituto de Bioquímica Médica Universidade Federal do Rio de Janeiro Cidade Universitária Rio de Janeiro Brazil
- 3Université Côte d'Azur, Centre Commun de Microscopie Appliquée (CCMA) Nice France
- 4Department of Biological Sciences, Escola Superior de Agricultura “Luiz de Queiroz” Universidade de São Paulo Piracicaba Brazil
Abstract
The anaphase‐promoting complex/cyclosome (APC/C) is a multi‐subunit E3 ubiquitin ligase that regulates cell cycle progression, but its role in plant‐pathogen interactions is poorly understood. Here, we demonstrate that regulation of the ubiquitin–proteasome system, involving APC/C‐associated components, is critical for coordinating host cell cycle modulation and cellular homoeostasis required for proper gall formation and successful nematode parasitism. Inhibition of the 26S proteasome with MG132 severely disrupted gall morphology and nematode development, indicating that proteasome activity is required for feeding site establishment and maintenance. To assess the contribution of APC/C associated components involved in proteasome‐mediated degradation, we examined the effects of overexpressing APC5, APC7 and APC10 during interactions with the root‐knot nematode Meloidogyne incognita and the oomycete Hyaloperonospora arabidopsidis (Hpa). Overexpression of a truncated APC7 variant (APC7‐CT OE), conferred strong resistance to both pathogens, reducing nematode egg mass production by 81% and Hpa conidiospore production by 97%. APC7‐CT OE plants exhibited altered gall morphology, suggesting premature senescence of giant cells. In contrast, overexpression of APC5 or APC10 increased susceptibility to M. incognita, revealing functional divergence among APC/C components. Our findings identify a previously unrecognised role for APC/C‐related regulatory pathways in regulating host cellular processes that influence pathogen success and highlight APC7‐CT as a potential target for improving resistance to diverse pathogens.
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BibTeX
@article{carneiro2026modulation,
title = {{Modulation of Anaphase‐Promoting Complex Genes Regulates Root‐Knot Nematode Gall Development and Plant Susceptibility}},
author = {Aline Köhn Carneiro and Kércya Maria Simões de Siqueira and La Hoang Anh and Sophie Pagnotta and Danila Cabral do Nascimento and Nubia Barbosa Eloy and Harald Keller and Adriana Silva Hemerly and Janice de Almeida Engler},
journal = {Plant, Cell \& Environment},
year = {2026},
month = sep,
doi = {10.1111/pce.70884},
url = {https://doi.org/10.1111/pce.70884},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Modulation of Anaphase‐Promoting Complex Genes Regulates Root‐Knot Nematode Gall Development and Plant Susceptibility
AU - Aline Köhn Carneiro
AU - Kércya Maria Simões de Siqueira
AU - La Hoang Anh
AU - Sophie Pagnotta
AU - Danila Cabral do Nascimento
AU - Nubia Barbosa Eloy
AU - Harald Keller
AU - Adriana Silva Hemerly
AU - Janice de Almeida Engler
PY - 2026
DA - 2026/09/22
JO - Plant, Cell & Environment
DO - 10.1111/pce.70884
UR - https://doi.org/10.1111/pce.70884
AB - The anaphase‐promoting complex/cyclosome (APC/C) is a multi‐subunit E3 ubiquitin ligase that regulates cell cycle progression, but its role in plant‐pathogen interactions is poorly understood. Here, we demonstrate that regulation of the ubiquitin–proteasome system, involving APC/C‐associated components, is critical for coordinating host cell cycle modulation and cellular homoeostasis required for proper gall formation and successful nematode parasitism. Inhibition of the 26S proteasome with MG132 severely disrupted gall morphology and nematode development, indicating that proteasome activity is required for feeding site establishment and maintenance. To assess the contribution of APC/C associated components involved in proteasome‐mediated degradation, we examined the effects of overexpressing APC5, APC7 and APC10 during interactions with the root‐knot nematode Meloidogyne incognita and the oomycete Hyaloperonospora arabidopsidis (Hpa). Overexpression of a truncated APC7 variant (APC7‐CT OE), conferred strong resistance to both pathogens, reducing nematode egg mass production by 81% and Hpa conidiospore production by 97%. APC7‐CT OE plants exhibited altered gall morphology, suggesting premature senescence of giant cells. In contrast, overexpression of APC5 or APC10 increased susceptibility to M. incognita, revealing functional divergence among APC/C components. Our findings identify a previously unrecognised role for APC/C‐related regulatory pathways in regulating host cellular processes that influence pathogen success and highlight APC7‐CT as a potential target for improving resistance to diverse pathogens.
SN - 0140-7791
SN - 1365-3040
ER -