TRAF6-dependent NF-kB transcriptional activity during mouse development

被引:54
作者
Dickson, KM [1 ]
Bhakar, AL [1 ]
Barker, PA [1 ]
机构
[1] McGill Univ, Montreal Neurol Inst, Ctr Neuronal Survival, Montreal, PQ H3A 2B4, Canada
关键词
TRAF; epithelium; endothelium; mammary gland; floor plate; roof plate; telencephalon;
D O I
10.1002/dvdy.20110
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 [人体解剖与组织胚胎学];
摘要
Nuclear factor-kappa B (NF-kB) transcriptional activity is induced by numerous stimuli. To identify tissues exhibiting NF-kB transcriptional activity during development, we analyzed transgenic reporter mice that express beta-galactosidase from an NF-kB-responsive element. We report that NF-kB activation is widespread and present in numerous epithelial structures and within vasculature. Several regions of the developing central nervous system, including the roof plate and floor plate of the midbrain, show prominent NF-kB activation. To assess the role of the TRAF6 adaptor protein in developmental NF-kB activity, we analyzed NF-kB activation in reporter mice rendered null for TRAF6. Deletion of TRAF6 resulted in the loss of NF-kB activity in epithelia, in vasculature, and in roof and floor plate but had no effect on NF-kB activity developing telencephalon, choroid plexus, cochlear canal, and thymus. These data indicate that NF-kB transcriptional activity is present in a broad range of structures during development and that TRAF6 plays a critical role mediating developmental NF-kB activation in many but not all tissues. (C) 2004 Wiley-Liss, Inc.
引用
收藏
页码:122 / 127
页数:6
相关论文
共 12 条
[1]
A RANK/TRAF6-dependent signal transduction pathway is essential for osteoclast cytoskeletal organization and resorptive function [J].
Armstrong, AP ;
Tometsko, ME ;
Glaccum, M ;
Sutherland, CL ;
Cosman, D ;
Dougall, WC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (46) :44347-44356
[2]
Bhakar AL, 2002, J NEUROSCI, V22, P8466
[3]
Tumor necrosis factor receptor-associated factors (TRAFs) [J].
Bradley, JR ;
Pober, JS .
ONCOGENE, 2001, 20 (44) :6482-6491
[4]
Chung JY, 2002, J CELL SCI, V115, P679
[5]
Missing pieces in the NF-κB puzzle [J].
Ghosh, S ;
Karin, M .
CELL, 2002, 109 :S81-S96
[6]
The Rel/NF-κB signal transduction pathway:: introduction [J].
Gilmore, TD .
ONCOGENE, 1999, 18 (49) :6842-6844
[7]
Phosphorylation meets ubiquitination:: The control of NF-κB activity [J].
Karin, M ;
Ben-Neriah, Y .
ANNUAL REVIEW OF IMMUNOLOGY, 2000, 18 :621-+
[8]
TRAF6 deficiency results in osteopetrosis and defective interleukin-1, CD40, and LPS signaling [J].
Lomaga, MA ;
Yeh, WC ;
Sarosi, I ;
Duncan, GS ;
Furlonger, C ;
Ho, A ;
Morony, S ;
Capparelli, C ;
Van, G ;
Kaufman, S ;
van der Heiden, A ;
Itie, A ;
Wakeham, A ;
Khoo, W ;
Sasaki, T ;
Cao, ZD ;
Penninger, JM ;
Paige, CJ ;
Lacey, DL ;
Dunstan, CR ;
Boyle, WJ ;
Goeddel, DV ;
Mak, TW .
GENES & DEVELOPMENT, 1999, 13 (08) :1015-1024
[9]
Lomaga MA, 2000, J NEUROSCI, V20, P7384
[10]
TRAF6-deficient mice display hypohidrotic ectodermal dysplasia [J].
Naito, A ;
Yoshida, H ;
Nishioka, E ;
Satoh, M ;
Azuma, S ;
Yamamoto, T ;
Nishikawa, S ;
Inoue, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (13) :8766-8771