|
|
Blood, 1 August 2007, Vol. 110, No. 3, pp. 870-876.
Prepublished online as a Blood First Edition Paper on April 12, 2007; DOI 10.1182/blood-2007-01-068528.
 Previous Article | Next Article 
Submitted January 17, 2007
Accepted April 9, 2007
Disruption of palladin leads to defects in definitive erythropoiesis by interfering erythroblastic island formation in mouse fetal liver
Xue-Song Liu, Xi-Hua Li, Yi Wang, Run-Zhe Shu, Long Wang, Shun-Yuan Lu, Hui Kong, Yue-E Jin, Li-Jun Zhang, Jian Fei, Sai-Juan Chen, Zhu Chen, Ming-Min Gu, Zhen-Yu Lu, and Zhu-Gang Wang*
Laboratory of Genetic Engineering, Dept of Medical Genetics, Inst .of Health Sciences, Shanghai Jiao Tong Univ. & Shanghai Inst. for Biological Sciences, Shanghai, China
Graduate School of Chinese Academy of Sciences, Shanghai, China
Shanghai Research Center for Model Organisms, Shanghai, China
State Key Laboratory of Medical Genomics, Rui-jin Hospital, Shanghai Jiao Tong University, Shanghai, China
* Corresponding author; email: zhugangw{at}shsmu.edu.cn.
Palladin was originally found up-regulated with NB4 cell differentiation induced by ATRA. Disruption of palladin results in neural tube closure defects, liver herniation and embryonic lethality. Here we further report that palladin-/- embryos exhibit a significant defect in erythropoiesis, characterized by dramatic reduction in definitive erythrocytes derived from fetal liver but not primitive erythrocytes from yolk sac. The reduction of erythrocytes is accompanied by increased apoptosis of erythroblasts and partial blockage of erythroid differentiation. However, colony forming assay shows no differences between wt and mutant fetal liver or yolk sac in the number and size of colonies tested. In addition, palladin-/- fetal liver cells can reconstitute hematopoiesis in lethally-irradiated mice. These data strongly suggest that deficient erythropoiesis in palladin-/- fetal liver is mainly due to compromised erythropoietic microenvironment. As expected, erythroblastic island in palladin-/- fetal liver was found disorganized. Palladin-/- fetal liver cells fail to form erythroblastic island in vitro. Interestingly, wt macrophages can form such units with either wt or mutant erythroblasts, while mutant macrophages lose their ability to bind wt or mutant erythroblasts. These data demonstrate that palladin is crucial for definitive erythropoiesis and erythroblastic island formation, and especially, required for normal function of macrophages in fetal liver.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
L. Jin, T. Yoshida, R. Ho, G. K. Owens, and A. V. Somlyo
The Actin-associated Protein Palladin Is Required for Development of Normal Contractile Properties of Smooth Muscle Cells Derived from Embryoid Bodies
J. Biol. Chem.,
January 23, 2009;
284(4):
2121 - 2130.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. A. Chasis and N. Mohandas
Erythroblastic islands: niches for erythropoiesis
Blood,
August 1, 2008;
112(3):
470 - 478.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. E. McGrath, P. D. Kingsley, A. D. Koniski, R. L. Porter, T. P. Bushnell, and J. Palis
Enucleation of primitive erythroid cells generates a transient population of "pyrenocytes" in the mammalian fetus
Blood,
February 15, 2008;
111(4):
2409 - 2417.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
