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Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection
08:16

Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection

Published on: July 21, 2022

Influenza A virus-induced caspase-3 cleaves the histone deacetylase 6 in infected epithelial cells

Matloob Husain1, Kevin S Harrod

  • 1Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA. mhusain@lrri.org

FEBS Letters
|July 15, 2009
PubMed

Insights

Histone deacetylase 6 (HDAC6) is cleaved by caspase-3 during influenza A virus (IAV) infection. This cleavage impacts HDAC6 function and may play a role in IAV-induced apoptosis.

Area of Science:

  • Molecular Biology
  • Virology
  • Cellular Biology

Background:

  • Histone deacetylase 6 (HDAC6) is a key cytoplasmic enzyme regulating diverse biological processes.
  • Emerging evidence suggests a role for HDAC6 in viral infections, but its regulation in infected cells remains unclear.
  • Understanding HDAC6 regulation during viral infection is crucial for elucidating host-pathogen interactions.

Purpose of the Study:

  • To investigate the post-translational modification and regulation of HDAC6 in influenza A virus (IAV)-infected cells.
  • To identify specific enzymes responsible for HDAC6 cleavage during IAV infection.
  • To determine the functional significance of HDAC6 cleavage in the context of IAV-induced apoptosis.

Main Methods:

  • Western blot analysis to detect cleaved HDAC6 in IAV-infected cells.
  • Identification of caspase-3 cleavage motif (DMAD-S) within the HDAC6 polypeptide.
  • In vitro assays to confirm HDAC6 as a direct substrate of caspase-3.

Main Results:

  • HDAC6 undergoes caspase-3-mediated cleavage in cells infected with influenza A virus.
  • The C-terminal ubiquitin-binding zinc finger domain of HDAC6 is removed upon cleavage.
  • HDAC6 is confirmed as a direct substrate of caspase-3, with a specific cleavage motif identified.

Conclusions:

  • Caspase-3 activation leads to the specific cleavage of HDAC6 during influenza A virus infection.
  • The cleavage of HDAC6 may alter its function and contribute to the apoptotic processes induced by IAV.
  • This study reveals a novel regulatory mechanism of HDAC6 in virus-infected cells, highlighting its potential role in viral pathogenesis.

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