Open AccessThe JNK/AP‐1 pathway upregulates expression of the recycling endosome rab11a gene in B cells transformed by Theileria
Author(s) -
Lizundia Regina,
Chaussepied Marie,
Naissant Bernina,
Masse Guillemette X.,
Quevillon Emmanuel,
Michel Fréderique,
Monier Solange,
Weitzman Jonathan B.,
Langsley Gordon
Publication year - 2007
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2007.00925.x
Subject(s) - endosome , microbiology and biotechnology , biology , downregulation and upregulation , gene knockdown , transcription factor , cell cycle , cell , cell culture , gene , biochemistry , intracellular , genetics
Summary Lymphocyte transformation induced by Theileria parasites involves constitutive activation of c‐Jun N‐terminal kinase (JNK) and the AP‐1 transcription factor. We found that JNK/AP‐1 activation is associated with elevated levels of Rab11 protein in Theileria ‐transformed B cells. We show that AP‐1 regulates rab11a promoter activity in B cells and that the induction of c‐Jun activity in mouse fibroblasts also leads to increased transcription of the endogenous rab11a gene, consistent with it being an AP‐1 target. Pharmacological inhibition of the JNK pathway reduced Rab11 protein levels and endosome recycling of transferrin receptor (TfR) and siRNA knockdown of JNK1 and Rab11A levels also reduced TfR surface expression. We propose a model, where activation of the JNK/AP‐1 pathway during cell transformation might assure that the regulation of recycling endosomes is co‐ordinated with cell‐cycle progression. This might be achieved via the simultaneous upregulation of the cell cycle machinery (e.g. cyclin D1) and the recycling endosome regulators (e.g. Rab11A).