Abstract
The BTB-POZ transcription factor Promyelocytic Leukemia Zinc Finger (PLZF, or ZBTB16) has been recently identified as a major factor regulating the induction of a subset of Interferon stimulated genes in human and mouse. We show that the two co-orthologues of PLZF found in zebrafish show distinct expression patterns, especially in larvae. Although zbtb16a/plzfa and zbtb16b/plzfb are not modulated by IFN produced during viral infection, their over-expression increases the level of the early type I IFN response, at a critical phase in the race between the virus and the host response. The effect of Plzfb on IFN induction was also detectable after cell infection by different non-enveloped RNA viruses, but not after infection by the rhabdovirus SVCV. Our findings indicate that plzf implication in the regulation of type I IFN responses is conserved across vertebrates, but at multiple levels of the pathway and through different mechanisms.
Original language | English |
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Pages (from-to) | 48-56 |
Number of pages | 9 |
Journal | Developmental and Comparative Immunology |
Volume | 57 |
DOIs | |
Publication status | Published - 1 Apr 2016 |
Externally published | Yes |
Keywords*
- Antiviral innate immunity
- Interferon
- PLZF
- ZBTB
- Zebrafish
Field of Science*
- 3.2 Clinical medicine
Publication Type*
- 1.1. Scientific article indexed in Web of Science and/or Scopus database