Journal home
Advance online publication
Current issue
Archive
Press releases
Focuses
Guide to authors
Online submissionOnline submission
For referees
Free online issue
Contact the journal
Subscribe
Advertising
work@npg
Reprints and permissions
About this site
For librarians
 
NPG Resources
Nature
Nature Reviews Immunology
Nature Medicine
Nature Cell Biology
NI Tutorial: Finding regulatory DNA regions
Signaling Gateway
Immunology & Cell Biology
Mucosal Immunology
Nature Conferences
Nature Stem Cells
NPG Subject areas
Biotechnology
Cancer
Chemistry
Clinical Medicine
Dentistry
Development
Drug Discovery
Earth Sciences
Evolution & Ecology
Genetics
Immunology
Materials Science
Medical Research
Microbiology
Molecular Cell Biology
Neuroscience
Pharmacology
Physics
Browse all publications
Article
Nature Immunology  4, 138 - 144 (2003)
Published online: 13 January 2003; | doi:10.1038/ni881

Impaired thymic development in mouse embryos deficient in apoptotic DNA degradation

Kohki Kawane1, Hidehiro Fukuyama1, 6, Hideyuki Yoshida1, Hiroko Nagase1, Yoshiyuki Ohsawa2, Yasuo Uchiyama2, Kazuhisa Okada3, Tetsuya Iida3 & Shigekazu Nagata1, 4, 5

1  Department of Genetics, Osaka University Medical School, Osaka 565-0871, Japan

2  Departments of Cell Biology and Neuroscience, Osaka University Medical School, Osaka 565-0871, Japan

3  Department of Bacterial Infections, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan

4  Laboratory of Genetics, Integrated Biology Laboratories, Graduate School of Frontier Biosciences, Osaka University, Osaka 565-0871, Japan

5  Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Osaka 565-0871, Japan

6  Present address: Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY 10021, USA.

Correspondence should be addressed to Shigekazu Nagata nagata@genetic.med.osaka-u.ac.jp
Apoptosis is often accompanied by the degradation of chromosomal DNA. Caspase-activated DNase (CAD) is an endonuclease that is activated in dying cells, whereas DNase II is present in the lysosomes of macrophages. Here, we show that CAD-/- thymocytes did not undergo apoptotic DNA degradation. But, when apoptotic cells were phagocytosed by macrophages, their DNA was degraded by DNase II. The thymus of DNase II-/-CAD-/- embryos contained many foci carrying undigested DNA and the cellularity was severely reduced due to a block in T cell development. The interferon-beta gene was strongly up-regulated in the thymus of DNase II-/-CAD-/- embryos, suggesting that when the DNA of apoptotic cells is left undigested, it can activate innate immunity leading to defects in thymic development.

MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated

REFERENCE
Thymus
Nature Encyclopaedia of Life Sciences
 See all 2 matches for Reference

REVIEWS
Degradation of chromosomal DNA during apoptosis
Cell Death and Differentiation Reviews (01 Jan 2003)
 See all 15 matches for Reviews

NEWS AND VIEWS
Control of apoptotic DNA degradation
Nature Cell Biology News and Views (01 Apr 2000)
Apoptosis: Condensed matter in cell death
Nature News and Views (09 Sep 1999)
 See all 4 matches for News And Views

RESEARCH
Macrophages are involved in DNA degradation of apoptotic cells in murine thymus after administration of hydrocortisone
Cell Death and Differentiation Original Article (01 Feb 2002)
 See all 40 matches for Research

 Top
Abstract
Previous | Next
Table of contents
Full textFull text
Download PDFDownload PDF
Send to a friendSend to a friend
Save this linkSave this link
Figures & Tables
Export citation
natureproducts

Search buyers guide:

 
ADVERTISEMENT
 
Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
Journal home | Advance online publication | Current issue | Archive | Press releases | Focuses | For authors | Online submission | Permissions | For referees | Free online issue | About the journal | Contact the journal | Subscribe | Advertising | work@npg | naturereprints | About this site | For librarians
Nature Publishing Group, publisher of Nature, and other science journals and reference works©2003 Nature Publishing Group | Privacy policy