Immobilized Subpopulations of Leaf Epidermal Mitochondria Mediate PENETRATION2-Dependent Pathogen Entry Control in

Rene Fuchs1, Michaela Kopischke1, Christine Klapprodt1

  • 1Department of Plant Cell Biology, Albrecht-von-Haller-Institute, Georg-August-University Göttingen, 37077 Göttingen, Germany The Sainsbury Laboratory, Norwich NR4 7UH, United Kingdom.

The Plant Cell
|January 2, 2016
PubMed

Insights

PENETRATION2 (PEN2) protein targets both peroxisomes and mitochondria, crucial for plant defense against fungal pathogens. Immobilized mitochondria at invasion sites accumulate PEN2, signaling pathogen attack.

Area of Science:

  • Plant pathology
  • Cell biology
  • Biochemistry

Background:

  • PENETRATION2 (PEN2) is an atypical myrosinase vital for plant immunity against filamentous pathogens.
  • Previous studies indicated PEN2-GFP localizes to peroxisomes, but its full targeting and function remained unclear.

Purpose of the Study:

  • To elucidate the precise subcellular localization and functional role of PEN2 in plant defense.
  • To investigate PEN2's interaction with other cellular components during pathogen invasion.

Main Methods:

  • Utilized GFP-tagged PEN2 to track its localization in plant cells using live-cell imaging.
  • Investigated PEN2's membrane targeting properties and homo-oligomerization capacity.
  • Analyzed mitochondrial dynamics and PEN2 accumulation at pathogen attack sites.

Main Results:

  • Demonstrated PEN2 is a tail-anchored protein with dual targeting to peroxisomes and mitochondria.
  • Showcased pathogen-induced recruitment and immobilization of mitochondria at fungal invasion sites, with PEN2 accumulation.
  • Confirmed that PEN2 targeting to the outer mitochondrial membrane rescues the pen2 mutant phenotype.

Conclusions:

  • PEN2's dual localization and mitochondrial targeting are critical for its function in plant defense.
  • Mitochondrial PEN2 facilitates localized production of defense compounds at pathogen interaction sites.
  • Pathogen-induced mitochondrial dysfunction and redox imbalance may generate crucial defense signals.