|
|
Blood, 1 July 2007, Vol. 110, No. 1, pp. 99-106.
Prepublished online as a Blood First Edition Paper on March 16, 2007; DOI 10.1182/blood-2006-11-059204.
Previous Article | Next Article 
Submitted November 22, 2006
Accepted March 9, 2007
The zebrafish udu gene encodes a novel nuclear factor and is essential for primitive erythroid cell development
Yanmei Liu, Linsen Du, Motomi Osato, Eng Hui Teo, Feng Qian, Hao Jin, Fenghua Zhen, Jin Xu, Lin Guo, Honghui Huang, Jun Chen, Robert Geisler, Yun-Jin Jiang, Jinrong Peng, and Zilong Wen*
Laboratory of Molecular & Developmental Immunology, Institute of Molecular and Cell Biology, Singapore
Department of Biological Sciences, The National University of Singapore, Singapore
Laboratory of molecular oncology, Institute of Molecular and Cell Biology, Singapore
Functional Genomics Laboratory, Institute of Molecular and Cell Biology, Singapore
Max Planck Institute fuer Entwicklungsbiologie, Tuebingen, Germany
Laboratory of Developmental Signalling & Patterning, Institute of Molecular and Cell Biology, Singapore
* Corresponding author; email: zilong{at}imcb.a-star.edu.sg.
Hematopoiesis is a complex process which gives rise to all blood lineages in the course of an organism's lifespan. Yet the underlying molecular mechanism governing this process is not fully understood. Here we report the isolation and detailed study of a newly identified zebrafish ugly duckling (udu) mutant allele, udusq1. We show that loss-of-function mutation in the udu gene disrupts primitive erythroid cell proliferation and differentiation in a cell-autonomous manner, resulting in red blood cell (RBC) hypoplasia. Positional cloning reveals that the udu gene encodes a novel factor that contains two Paired Amphipathic -Helix like (PAH-L) repeats and a putative SW13, ADA2, N-Cor and TFIIIB like (SANT-L) domain. We further show that the Udu protein is predominantly localized in the nucleus and deletion of the putative SANT-L domain abolishes its function. Our study indicates that the Udu protein is very likely to function as a transcription modulator essential for the proliferation and differentiation of erythroid lineage.

CiteULike Connotea Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
C.-H. Lim, S.-W. Chong, and Y.-J. Jiang
Udu Deficiency Activates DNA Damage Checkpoint
Mol. Biol. Cell,
October 1, 2009;
20(19):
4183 - 4193.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
F. Guillem, S. Lawson, C. Kannengiesser, M. Westerman, C. Beaumont, and B. Grandchamp
Two nonsense mutations in the TMPRSS6 gene in a patient with microcytic anemia and iron deficiency
Blood,
September 1, 2008;
112(5):
2089 - 2091.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
D. Carradice and G. J. Lieschke
Zebrafish in hematology: sushi or science?
Blood,
April 1, 2008;
111(7):
3331 - 3342.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|
|