Opposite functions of Jun‐B and c‐jun in growth regulation and neuronal differentiation

Opposite functions of Jun‐B and c‐jun in growth regulation and neuronal differentiation Induction of the jun‐B and/or c‐jun transcription factors is part of the immediate early response to diverse stimuli that induce alterations in cellular programs. While c‐jun is a protooncogene whose expression is required for induction of cell proliferation, jun‐B has recently been found to be induced by stimuli inducing differentiation in various cell lines. Furthermore, its expression is largely restricted to differentiating cells during embryogenesis. To determine the functional significance of these findings, we used antisense phosphorothioate oligodeoxynucleotides to inhibit expression of the two genes in proliferating and neuronally differentiating cells. While selective inhibition of c‐jun expression reduced proliferation rates, inhibition of jun‐B protein synthesis markedly increased proliferation in 3T3 fibroblasts, human mammary carcinoma cells and PC‐12 pheochromocytoma cells, suggesting jun‐B involvement in negative growth control. Neuronal differentiation of PC‐12 cells induced by nerve growth factor (NGF) was prevented by inhibition of jun‐B protein synthesis. PC‐12 cells not only failed to grow neurites but also remained in the proliferative state. Furthermore, in cultured primary neurons from rat hippocampus, inhibition of jun‐B expression, again, markedly reduced morphological differentiation. Conversely, inhibition of c‐jun protein synthesis enhanced morphological differentiation of both primary neurons and PC‐12 tumor cells. Thus, jun‐B expression is required for neuronal differentiation and its balance with c‐jun activity is involved in regulating key steps in proliferation and differentiation processes. © 1993Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genesis: the Journal of Genetics and Development Wiley

Loading next page...
 
/lp/wiley/opposite-functions-of-jun-b-and-c-jun-in-growth-regulation-and-05KmpORBxm
Publisher
Wiley
Copyright
"Copyright © 1993 Wiley Subscription Services, Inc., A Wiley Company"
ISSN
1526-954X
eISSN
1526-968X
D.O.I.
10.1002/dvg.1020140408
Publisher site
See Article on Publisher Site

Abstract

Induction of the jun‐B and/or c‐jun transcription factors is part of the immediate early response to diverse stimuli that induce alterations in cellular programs. While c‐jun is a protooncogene whose expression is required for induction of cell proliferation, jun‐B has recently been found to be induced by stimuli inducing differentiation in various cell lines. Furthermore, its expression is largely restricted to differentiating cells during embryogenesis. To determine the functional significance of these findings, we used antisense phosphorothioate oligodeoxynucleotides to inhibit expression of the two genes in proliferating and neuronally differentiating cells. While selective inhibition of c‐jun expression reduced proliferation rates, inhibition of jun‐B protein synthesis markedly increased proliferation in 3T3 fibroblasts, human mammary carcinoma cells and PC‐12 pheochromocytoma cells, suggesting jun‐B involvement in negative growth control. Neuronal differentiation of PC‐12 cells induced by nerve growth factor (NGF) was prevented by inhibition of jun‐B protein synthesis. PC‐12 cells not only failed to grow neurites but also remained in the proliferative state. Furthermore, in cultured primary neurons from rat hippocampus, inhibition of jun‐B expression, again, markedly reduced morphological differentiation. Conversely, inhibition of c‐jun protein synthesis enhanced morphological differentiation of both primary neurons and PC‐12 tumor cells. Thus, jun‐B expression is required for neuronal differentiation and its balance with c‐jun activity is involved in regulating key steps in proliferation and differentiation processes. © 1993Wiley‐Liss, Inc.

Journal

Genesis: the Journal of Genetics and DevelopmentWiley

Published: Jan 1, 1993

Keywords: ; ; ; ; ;

References

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create folders to
organize your research

Export folders, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off