The Wave2 scaffold Hem-1 is required for transition of fetal liver hematopoiesis to bone marrow

Lijian Shao, Jianhui Chang, Wei Feng, Xiaoyan Wang, Elizabeth A. Williamson, Ying Li, Amir Schajnovitz, David Scadden, Luke J. Mortensen, Charles P. Lin, Linheng Li, Ariel Paulson, James Downing, Daohong Zhou () and Robert A. Hromas ()
Additional contact information
Lijian Shao: University of Illinois Chicago
Jianhui Chang: University of Arkansas for Medical Sciences
Wei Feng: University of Arkansas for Medical Sciences
Xiaoyan Wang: University of Arkansas for Medical Sciences
Elizabeth A. Williamson: University of Florida
Ying Li: University of Florida
Amir Schajnovitz: Harvard University
David Scadden: Harvard University
Luke J. Mortensen: University of Georgia
Charles P. Lin: Harvard Medical School
Linheng Li: Medicine University of Kansas
Ariel Paulson: Medicine University of Kansas
James Downing: St. Jude Children’s Research Hospital
Daohong Zhou: University of Arkansas for Medical Sciences
Robert A. Hromas: University of Texas Health Science Center

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract The transition of hematopoiesis from the fetal liver (FL) to the bone marrow (BM) is incompletely characterized. We demonstrate that the Wiskott–Aldrich syndrome verprolin-homologous protein (WAVE) complex 2 is required for this transition, as complex degradation via deletion of its scaffold Hem-1 causes the premature exhaustion of neonatal BM hematopoietic stem cells (HSCs). This exhaustion of BM HSC is due to the failure of BM engraftment of Hem-1−/− FL HSCs, causing early death. The Hem-1−/− FL HSC engraftment defect is not due to the lack of the canonical function of the WAVE2 complex, the regulation of actin polymerization, because FL HSCs from Hem-1−/− mice exhibit no defects in chemotaxis, BM homing, or adhesion. Rather, the failure of Hem-1−/− FL HSC engraftment in the marrow is due to the loss of c-Abl survival signaling from degradation of the WAVE2 complex. However, c-Abl activity is dispensable for the engraftment of adult BM HSCs into the BM. These findings reveal a novel function of the WAVE2 complex and define a mechanism for FL HSC fitness in the embryonic BM niche.

Date: 2018
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-018-04716-5 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04716-5

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-018-04716-5

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().