Characterization of a Very Short Meq Protein Isoform in a Marek’s Disease Virus Strain in Japan

Author:

Motai Yoshinosuke1,Murata Shiro12ORCID,Sato Jumpei1,Nishi Akihito3,Maekawa Naoya2,Okagawa Tomohiro2ORCID,Konnai Satoru124,Ohashi Kazuhiko125

Affiliation:

1. Laboratory of Infectious Diseases, Department of Disease Control, Faculty of Veterinary Medicine, Hokkaido University, Kita-18, Nishi-9, Kita-ku, Sapporo 060-0818, Japan

2. Department of Advanced Pharmaceutics, Faculty of Veterinary Medicine, Hokkaido University, Kita-18, Nishi-9, Kita-ku, Sapporo 060-0818, Japan

3. Chuo Livestock Hygiene Service Center, Agriculture Promotion Department, Kochi Prefecture, 3229 Otsu, Takaoka-cho, Tosa 781-1102, Japan

4. Institute for Vaccine Research and Development (HU-IVReD), Hokkaido University, Kita-18, Nishi-9, Kita-ku, Sapporo 060-0818, Japan

5. International Affairs Office, Faculty of Veterinary Medicine, Hokkaido University, Kita-18, Nishi-9, Kita-ku, Sapporo 060-0818, Japan

Abstract

Marek’s disease virus (MDV) causes malignant lymphoma (Marek’s disease; MD) in chickens. The Meq protein is essential for tumorigenesis since it regulates the expression of host and viral genes. Previously, we reported that the deletion of the short isoform of Meq (S-Meq) decreases the pathogenicity of MDV. Recently, we identified a further short isoform of Meq (very short isoform of Meq, VS-Meq) in chickens with MD in Japan. A 64-amino-acid deletion was confirmed at the C-terminus of VS-Meq. We measured the transcriptional regulation by VS-Meq in three gene promoters to investigate the effect of VS-Meq on protein function. Wild-type VS-Meq decreased the transrepression of the pp38 promoter but did not alter the transactivation activity of the Meq and Bcl-2 promoters. The deletion in VS-Meq did not affect the activity of the pp38 promoter but enhanced the transactivation activities of the Meq and Bcl-2 promoters. Collectively, the deletion of VS-Meq potentially enhanced the activity of the Meq promoter, while other amino acid sequences in wild-type VS-Meq seemed to affect the weak transrepression of the pp38 promoter. Further investigation is required to clarify the effects of these changes on pathogenicity.

Funder

Grants-in-Aid for Scientific Research

Grant-in-Aid for Challenging Research

Japan Society for the Promotion of Science

Publisher

MDPI AG

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