A nuclear fraction of turnip crinkle virus capsid protein is important for elicitation of the host resistance response

Sung Hwan Kang, Feng Qu, T. Jack Morris

Research output: Contribution to journalArticle

Abstract

The N-terminal 25 amino acids (AAs) of turnip crinkle virus (TCV) capsid protein (CP) are recognized by the resistance protein HRT to trigger a hypersensitive response (HR) and systemic resistance to TCV infection. This same region of TCV CP also contains a motif that interacts with the transcription factor TIP, as well as a nuclear localization signal (NLS). However, it is not yet known whether nuclear localization of TCV CP is needed for the induction of HRT-mediated HR and resistance. Here we present new evidence suggesting a tight correlation between nuclear inclusions formed by CP and the manifestation of HR. We show that a fraction of TCV CP localized to cell nuclei to form discrete inclusion-like structures, and a mutated CP (R6A) known to abolish HR failed to form nuclear inclusions. Notably, TIP-CP interaction augments the inclusion-forming activity of CP by tethering inclusions to the nuclear membrane. This TIP-mediated augmentation is also critical for HR resistance, as another CP mutant (R8A) known to elicit a less restrictive HR, though still self-associated into nuclear inclusions, failed to direct inclusions to the nuclear membrane due to its inability to interact with TIP. Finally, exclusion of CP from cell nuclei abolished induction of HR. Together, these results uncovered a strong correlation between nuclear localization and nuclear inclusion formation by TCV CP and induction of HR, and suggest that CP nuclear inclusions could be the key trigger of the HRT-dependent, yet TIP-reinforced, resistance to TCV.

Original languageEnglish (US)
Pages (from-to)264-270
Number of pages7
JournalVirus Research
Volume210
DOIs
StatePublished - Dec 2 2015

Fingerprint

Carmovirus
Capsid Proteins
Intranuclear Inclusion Bodies
Nuclear Envelope
Cell Nucleus
Nuclear Localization Signals
Virus Diseases

Keywords

  • Antiviral defense
  • Carmovirus
  • GFP
  • Nuclear localization
  • Plant virus
  • Resistance gene
  • Turnip crinkle virus

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases
  • Cancer Research

Cite this

A nuclear fraction of turnip crinkle virus capsid protein is important for elicitation of the host resistance response. / Kang, Sung Hwan; Qu, Feng; Morris, T. Jack.

In: Virus Research, Vol. 210, 02.12.2015, p. 264-270.

Research output: Contribution to journalArticle

@article{32e1b1e4bb064481a06d6568777523a0,
title = "A nuclear fraction of turnip crinkle virus capsid protein is important for elicitation of the host resistance response",
abstract = "The N-terminal 25 amino acids (AAs) of turnip crinkle virus (TCV) capsid protein (CP) are recognized by the resistance protein HRT to trigger a hypersensitive response (HR) and systemic resistance to TCV infection. This same region of TCV CP also contains a motif that interacts with the transcription factor TIP, as well as a nuclear localization signal (NLS). However, it is not yet known whether nuclear localization of TCV CP is needed for the induction of HRT-mediated HR and resistance. Here we present new evidence suggesting a tight correlation between nuclear inclusions formed by CP and the manifestation of HR. We show that a fraction of TCV CP localized to cell nuclei to form discrete inclusion-like structures, and a mutated CP (R6A) known to abolish HR failed to form nuclear inclusions. Notably, TIP-CP interaction augments the inclusion-forming activity of CP by tethering inclusions to the nuclear membrane. This TIP-mediated augmentation is also critical for HR resistance, as another CP mutant (R8A) known to elicit a less restrictive HR, though still self-associated into nuclear inclusions, failed to direct inclusions to the nuclear membrane due to its inability to interact with TIP. Finally, exclusion of CP from cell nuclei abolished induction of HR. Together, these results uncovered a strong correlation between nuclear localization and nuclear inclusion formation by TCV CP and induction of HR, and suggest that CP nuclear inclusions could be the key trigger of the HRT-dependent, yet TIP-reinforced, resistance to TCV.",
keywords = "Antiviral defense, Carmovirus, GFP, Nuclear localization, Plant virus, Resistance gene, Turnip crinkle virus",
author = "Kang, {Sung Hwan} and Feng Qu and Morris, {T. Jack}",
year = "2015",
month = "12",
day = "2",
doi = "10.1016/j.virusres.2015.08.014",
language = "English (US)",
volume = "210",
pages = "264--270",
journal = "Virus Research",
issn = "0168-1702",
publisher = "Elsevier",

}

TY - JOUR

T1 - A nuclear fraction of turnip crinkle virus capsid protein is important for elicitation of the host resistance response

AU - Kang, Sung Hwan

AU - Qu, Feng

AU - Morris, T. Jack

PY - 2015/12/2

Y1 - 2015/12/2

N2 - The N-terminal 25 amino acids (AAs) of turnip crinkle virus (TCV) capsid protein (CP) are recognized by the resistance protein HRT to trigger a hypersensitive response (HR) and systemic resistance to TCV infection. This same region of TCV CP also contains a motif that interacts with the transcription factor TIP, as well as a nuclear localization signal (NLS). However, it is not yet known whether nuclear localization of TCV CP is needed for the induction of HRT-mediated HR and resistance. Here we present new evidence suggesting a tight correlation between nuclear inclusions formed by CP and the manifestation of HR. We show that a fraction of TCV CP localized to cell nuclei to form discrete inclusion-like structures, and a mutated CP (R6A) known to abolish HR failed to form nuclear inclusions. Notably, TIP-CP interaction augments the inclusion-forming activity of CP by tethering inclusions to the nuclear membrane. This TIP-mediated augmentation is also critical for HR resistance, as another CP mutant (R8A) known to elicit a less restrictive HR, though still self-associated into nuclear inclusions, failed to direct inclusions to the nuclear membrane due to its inability to interact with TIP. Finally, exclusion of CP from cell nuclei abolished induction of HR. Together, these results uncovered a strong correlation between nuclear localization and nuclear inclusion formation by TCV CP and induction of HR, and suggest that CP nuclear inclusions could be the key trigger of the HRT-dependent, yet TIP-reinforced, resistance to TCV.

AB - The N-terminal 25 amino acids (AAs) of turnip crinkle virus (TCV) capsid protein (CP) are recognized by the resistance protein HRT to trigger a hypersensitive response (HR) and systemic resistance to TCV infection. This same region of TCV CP also contains a motif that interacts with the transcription factor TIP, as well as a nuclear localization signal (NLS). However, it is not yet known whether nuclear localization of TCV CP is needed for the induction of HRT-mediated HR and resistance. Here we present new evidence suggesting a tight correlation between nuclear inclusions formed by CP and the manifestation of HR. We show that a fraction of TCV CP localized to cell nuclei to form discrete inclusion-like structures, and a mutated CP (R6A) known to abolish HR failed to form nuclear inclusions. Notably, TIP-CP interaction augments the inclusion-forming activity of CP by tethering inclusions to the nuclear membrane. This TIP-mediated augmentation is also critical for HR resistance, as another CP mutant (R8A) known to elicit a less restrictive HR, though still self-associated into nuclear inclusions, failed to direct inclusions to the nuclear membrane due to its inability to interact with TIP. Finally, exclusion of CP from cell nuclei abolished induction of HR. Together, these results uncovered a strong correlation between nuclear localization and nuclear inclusion formation by TCV CP and induction of HR, and suggest that CP nuclear inclusions could be the key trigger of the HRT-dependent, yet TIP-reinforced, resistance to TCV.

KW - Antiviral defense

KW - Carmovirus

KW - GFP

KW - Nuclear localization

KW - Plant virus

KW - Resistance gene

KW - Turnip crinkle virus

UR - http://www.scopus.com/inward/record.url?scp=84947811413&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84947811413&partnerID=8YFLogxK

U2 - 10.1016/j.virusres.2015.08.014

DO - 10.1016/j.virusres.2015.08.014

M3 - Article

C2 - 26299399

AN - SCOPUS:84947811413

VL - 210

SP - 264

EP - 270

JO - Virus Research

JF - Virus Research

SN - 0168-1702

ER -