Cited by 15Fungal Plant Pathogen ControlPlant Pathogens and Fungal DiseasesPlant Disease Resistance and Genetics

A melanin-deficient isolate of Venturia inaequalis reveals various roles of melanin in pathogen life cycle and fitness

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Steiner, Ulrike, Oerke, Erich-Christian·2022·Journal of Fungi

Abstract

Venturia inaequalis is the ascomycetous pathogen causing apple scabs and forms dark-pigmented spores and partially melanised infection structures. Although melanin is considered to be essential for the infection of host tissue, a spontaneously occurring melanin-deficient mutant was isolated from an abaxial side of an apple leaf and can be cultivated in vitro as well as in vivo. The morphology and development of the melanin-deficient-isolate SW01 on leaves of susceptible apple plants were compared to that of the corresponding wild-type isolate HS1. White conidia of SW01 were often wrinkled when dry and significantly increased their volume in suspension. Germination and formation of germtubes and appressoria were not impaired; however, the lack of melanisation of the appressorial ring structure at the interface with the plant cuticle significantly reduced the infection success of SW01. The colonisation of leaf tissue by non-melanised subcuticular hyphae was not affected until the initiation of conidiogenesis. Non-melanised conidiophores penetrated the plant cuticle from inside less successfully than the wild type, and the release of white conidia from less solid conidiophores above the cuticle was less frequent. Melanin in the outer cell wall of V. inaequalis was not required for the survival of conidia under ambient temperature or at −20 °C storage conditions, however, promoted the tolerance of the pathogen to copper and synthetic fungicides affecting the stability and function of the fungal cell wall, plasma membrane, respiration (QoIs) and enzyme secretion, but had no effect on the sensitivity to sulphur and SDHIs. The roles of melanin in different steps of the V. inaequalis life cycle and the epidemiology of apple scabs are discussed.

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  • Melanin-deficient mutant strains lose their pathogenic capacity due to compromised turgor pressure.

    “Melanin-deficient mutant strains lose their pathogenic capacity due to compromised turgor pressure, thereby highlighting the essential role of melanin [13,14].”

    From Fungal Melanin in Plant Pathogens: Complex Biosynthesis Pathways and Diverse Biological Functions (2025) · cites this paper as [13]

    The Discussion says the melanin-deficient isolate had reduced aggressiveness, but explicitly did not lose pathogenicity completely. It attributes reduced penetration success to poor concentration of cuticle-degrading enzymes and says physical force is not suitable for penetration; it does not attribute the effect to compromised turgor pressure. The supplied copy gives section labels but no page numbers. (LLM, conf=0.90)

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Cited by

Sorted by citations

Authors
Steiner, U., & Oerke, E.-C.
Affiliations
University of Bonn (DE)
Corresponding author
Oerke, Erich-Christian
Venue
Journal of Fungi
Publisher
MDPI AG
Published
2022-12-25
Volume
9
Issue
1
Pages
35
ISSN
2309-608X (ISSN-L)
OpenAlex
W4313244530
Cited by
15
References
1
Citations by year
2026: 4 · 2025: 5 · 2024: 5 · 2023: 1
FWCI
2.28
Type
journal article
Language
en
Open access
Locations
  • Journal of Fungi (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Topics
  • Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Fungal Plant Pathogen Control
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Plant Pathogens and Fungal Diseases
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Plant Disease Resistance and Genetics
Keywords
Venturia inaequalis, melanin, apple scab, appressoria, plant cuticle, pathogen fitness, conidial viability, fungicide resistance, copper tolerance, QoI fungicides, SDHI fungicides, enzyme secretion

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