Evidence map›Paper›PMID 42108495›Full record

ArticlePest management science2026

Comparative transcriptomics reveal distinct anthracnose immune pathways in resistant and susceptible Camellia oleifera clones.

Linzhe Yan, Xiaojie Peng, Cai Kai, Lifeng Zhou, Sanushka Naidoo, Haonan Wang, Xudong Zhou

Abstract readComparative Study
In one paragraph

Article in Pest management science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Linzhe YanState Key Laboratory for Development and Utilization of Forest Food Resources, College of Forestry and Biotechnology, Zhejiang A & F University, Hangzhou, China.ORCID https://orcid.org/0009-0006-1688-1844
Xiaojie PengState Key Laboratory for Development and Utilization of Forest Food Resources, College of Forestry and Biotechnology, Zhejiang A & F University, Hangzhou, China.
Cai KaiQingtian County Forestry Burea, Lishui, China.
Lifeng ZhouState Key Laboratory for Development and Utilization of Forest Food Resources, College of Forestry and Biotechnology, Zhejiang A & F University, Hangzhou, China.ORCID https://orcid.org/0000-0003-4922-4710
Sanushka NaidooDepartment of Biochemistry, Genetics and Microbiology, Forestry and Agricultural Biotechnology Institute (FABI), University of Pretoria, Pretoria, South Africa.
Haonan WangState Key Laboratory for Development and Utilization of Forest Food Resources, College of Forestry and Biotechnology, Zhejiang A & F University, Hangzhou, China.
Xudong ZhouState Key Laboratory for Development and Utilization of Forest Food Resources, College of Forestry and Biotechnology, Zhejiang A & F University, Hangzhou, China.

Funding

Launching Funds for Talents of Zhejiang A & F University 2020FR036Launching Funds for Talents of Zhejiang A & F University 2022LFR0005
6 · The paper itself

Abstract

backgroundCamellia oleifera is an important woody-oil crop in China. Camellia anthracnose caused by fungal species in the genus Colletotrichum severely affects the oil yield and quality. Disease-resistant Ca. oleifera clones have been developed while the molecular mechanism underlying anthracnose resistance remains unclear. This study aimed to uncover the key genes and regulatory networks mediating anthracnose resistance among different Ca. oleifera clones.

resultsComparative transcriptomic analysis of a highly-resistant Ca. oleifera clone (ChangLin 18) and a susceptible clone (ChangLin 40) revealed that host resistance to anthracnose is associated with rapid ROS accumulation, hypersensitive response (HR), and activation of defense-related pathways. These findings demonstrated differentially expressed genes enriched in signal transduction, hormone response, and redox regulation. Weighted gene co-expression network analysis (WGCNA) highlighted a core regulatory module comprising MYB and bHLH transcription factors and the hub gene CASP. Functional validation via transient silencing of Casparian Strip genes (CASP) in Nicotiana benthamiana impaired root development and increased susceptibility to anthracnose.

conclusionDisease resistance in Ca. oleifera arises from a multi-layered defense network integrating ROS homeostasis, hormone signaling, and transcriptional regulation. Our study identified the functionally validated CASP gene, as well as candidate MYB and bHLH transcription factors, as key regulators of anthracnose resistance. These findings offer valuable targets for advancing molecular breeding and sustainable disease control strategies in Ca. oleifera. © 2026 Society of Chemical Industry.

Indexed as

CamelliaColletotrichumDisease ResistancePlant DiseasesTranscriptomeGene Expression ProfilinganthracnoseCamellia oleiferapathwaysplant immuneresistance breeding

Identifiers

PMID42108495
PMCPMC13453193

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.