Scholarlink

Background <p>Fully mycoheterotrophic orchids depend entirely on fungal partners for carbon and mineral nutrition, yet the structural mechanisms that regulate fungal accommodation within host tissues remain poorly understood. This question is particularly relevant in the <i>Gastrodia elata-Armillaria</i> symbiosis, where the fungal partner is a wood-decaying basidiomycete capable of aggressive host colonization and responsible for root rot disease in many tree species. Here, we examined whether host cell wall remodeling and extensin deposition contribute to the establishment and regulation of the host-fungus interface in <i>G. elata</i> tubers.</p> Results <p>Ultrastructural analyses revealed extensive host-derived cell wall remodeling during fungal colonization of <i>G. elata</i> tubers, including localized wall thickening and the formation of hypha-encasing wall domains within fungal-colonized cells and adjacent boundary cells. Comprehensive Microarray Polymer Profiling identified extensin epitopes recognized by JIM20 as the most strongly enriched hydroxyproline-rich glycoproteins component following colonization. Immunogold labeling localized extensin-enriched HRGPs specifically to modified host cell walls and interfacial matrices surrounding intracellular hyphae. Quantitative comparison demonstrated that the interfacial matrix surrounding intracellular hyphae was substantially thicker than that reported for arbuscular or typical orchid mycorrhizal associations. Chemical inhibition of HRGPs deposition using 3,4-DHP disrupted interfacial wall formation, resulting in uncontrolled fungal spread into normally restricted tissues, cortical necrosis, and reduced tuber growth.</p> Conclusions <p>Our findings demonstrate that extensin-enriched host cell wall remodeling establishes a reinforced symbiotic interface that spatially restricts fungal invasion while maintaining potential routes for nutrient exchange. Our results reveal a structural mechanism enabling a fully mycoheterotrophic orchid to accommodate an invasive fungal symbiont, indicating that spatial compartmentalization of host-fungus interactions represents an important mechanism contributing to symbiotic stability.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Extensin-enriched host cell wall specialization restricts fungal invasion while sustaining symbiosis in the mycoheterotrophic orchid, Gastrodia elata

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月18日

查看全文
  • Yi-Tse Wang,
  • Bodil Jørgensen,
  • Chieh-Yun Cheng,
  • Chih-Hsin Yeh,
  • Yung-I Lee

摘要

Background

Fully mycoheterotrophic orchids depend entirely on fungal partners for carbon and mineral nutrition, yet the structural mechanisms that regulate fungal accommodation within host tissues remain poorly understood. This question is particularly relevant in the Gastrodia elata-Armillaria symbiosis, where the fungal partner is a wood-decaying basidiomycete capable of aggressive host colonization and responsible for root rot disease in many tree species. Here, we examined whether host cell wall remodeling and extensin deposition contribute to the establishment and regulation of the host-fungus interface in G. elata tubers.

Results

Ultrastructural analyses revealed extensive host-derived cell wall remodeling during fungal colonization of G. elata tubers, including localized wall thickening and the formation of hypha-encasing wall domains within fungal-colonized cells and adjacent boundary cells. Comprehensive Microarray Polymer Profiling identified extensin epitopes recognized by JIM20 as the most strongly enriched hydroxyproline-rich glycoproteins component following colonization. Immunogold labeling localized extensin-enriched HRGPs specifically to modified host cell walls and interfacial matrices surrounding intracellular hyphae. Quantitative comparison demonstrated that the interfacial matrix surrounding intracellular hyphae was substantially thicker than that reported for arbuscular or typical orchid mycorrhizal associations. Chemical inhibition of HRGPs deposition using 3,4-DHP disrupted interfacial wall formation, resulting in uncontrolled fungal spread into normally restricted tissues, cortical necrosis, and reduced tuber growth.

Conclusions

Our findings demonstrate that extensin-enriched host cell wall remodeling establishes a reinforced symbiotic interface that spatially restricts fungal invasion while maintaining potential routes for nutrient exchange. Our results reveal a structural mechanism enabling a fully mycoheterotrophic orchid to accommodate an invasive fungal symbiont, indicating that spatial compartmentalization of host-fungus interactions represents an important mechanism contributing to symbiotic stability.