The Lysine Methyltransferase SMYD2 Is Required for Definite Hematopoietic Stem Cell Production in the Mouse Embryo

被引：2
作者：
Edwards, Melissa A. [1 ,2 ]
Brown, Mark A. [1 ,3 ]
Alshiraihi, Ilham [1 ]
Jarrell, Dillon K. [4 ]
Tucker, Haley O. [2 ]
机构：
[1] Colorado State Univ, Cell & Mol Biol Program, Ft Collins, CO 80523 USA
[2] Univ Texas Austin, Dept Mol Biosci, 1 Univ Stn A5000, Austin, TX 78712 USA
[3] Colorado State Univ, Dept Clin Sci, Ft Collins, CO 80523 USA
[4] Univ Colorado, Dept Bioengn, Anschutz Med Campus, Aurora, CO 80045 USA
来源：
VETERINARY SCIENCES | 2020年 / 7卷 / 03期
基金：
美国国家科学基金会;
关键词：
SMYD2; hematopoietic; stem cells; mouse embryo; AORTIC ENDOTHELIUM; PATHWAY; METHYLATION;
D O I：
10.3390/vetsci7030100
中图分类号：
S85 [动物医学（兽医学）];
学科分类号：
0906 ;
摘要：
The five-membered SET and MYND domain-containing lysine methyltransferase (SMYD) family plays pivotal roles in development and differentiation. Initially characterized within the cardiovascular system, one such member, SMYD2, has been implicated in transcriptional and apoptotic regulation of hematopoiesis. Deletion ofSmyd2in adult mouse Hemaopoietic Stem Cells (HSC) using an interferon-induciblemx1-Cre-mediated conditional knockout (CKO) led to HSC reduction via both apoptosis and transcriptional deficiencies. Since HSC are specified from hemogenic endothelial (HE) cells in the dorsal aorta (DA), we sought to determine whether the flaw in HSC originated embryologically from this site. Toward this end, we performed deletion withvav-Cre mice, which is active in all hematopoietic and endothelial tissues from E10.5 embryonic life onward. Unexpectedly, we observed no defects in the embryo, other than apoptotic loss of definite HSC, whereas adult hematopoietic populations downstream were unaffected. These results further establish the importance of SMYD2 in antiapoptotic gene control of gene expression from the embryo to the adult.
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页数：7
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