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Regulation of basal cell plasticity by epidermal growth factor (EGF) and c‐Src in vivo in the mouse epididymis
Author(s) -
Roy Jeremy,
Ruan Ye Chun,
Hill Eric,
Visconti Pablo,
Krapf Dario,
Vinegoni Claudio,
Breton Sylvie
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.734.12
Subject(s) - microbiology and biotechnology , epidermal growth factor , biology , proto oncogene tyrosine protein kinase src , genetically modified mouse , gefitinib , tyrosine kinase , in vivo , keratin 5 , ex vivo , basal (medicine) , phosphorylation , transgene , endocrinology , receptor , epidermal growth factor receptor , signal transduction , immunology , biochemistry , immunohistochemistry , gene , insulin
Epididymal basal cells (BCs) sense the luminal environment by sending cell body projections that cross the tight‐junction barrier. BCs express the EGF receptor and its associated tyrosine kinase, c‐ Src, and we examined their role in their luminal sensing ability. BCs were visualized by in vivo multiphoton microscopy in our newly generated transgenic mice (KR5‐tdTomato), which express tdTomato exclusively in BCs. We found that BCs periodically elongate and retract their luminal‐reaching projections. Laser scanning confocal microscopy followed by 3D modeling showed that in vivo treatment with EGF (1 μM) or the EGFR inhibitor, Gefitinib (200 mg/kg/day), increased and decreased the number of luminal‐reaching BCs (labeled for keratin 5), respectively. Local EGF injection induced an increase in ERK1/2 phosphorylation. BCs in c‐Src knockout mice, which are infertile, exhibited no luminal‐reaching projections. We propose that EGF/EGFR/ERK1/2, together with c‐Src, are positive regulators of the luminal‐reaching property of BCs. A better understanding of the novel sensory function of BCs in the epididymis will help define their role in male fertility. This study is supported by NIH grant RO1DK085715.