Deficiency of MIWI2 (Piwil4) induces mouse erythroleukemia cell differentiation, but has no effect on hematopoiesis in vivo.
Deficiency of MIWI2 (Piwil4) induces mouse erythroleukemia cell differentiation, but has no effect on hematopoiesis in vivo.
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DOI：
10.1371/journal.pone.0082573
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Martin DI
中科院分区：
文献类型：
--
作者：
Jacobs JE;Wagner M;Dhahbi J;Boffelli D;Martin DI
Piwi蛋白及其小的非编码RNA伴侣参与维持哺乳动物雄性生殖细胞中的干细胞特征和基因组完整性。MIWI 2是小鼠Piwi样蛋白之一，在精子发生的前粗线期从头甲基化期间表达。这种蛋白质的缺乏导致减数分裂缺陷和生殖细胞的逐渐丧失。越来越多的证据表明Piwi蛋白可能在造血组织中具有活性。因此，MIWI 2可能在造血干细胞和/或祖细胞自我更新和分化中起作用，并且MIWI 2的缺陷可能导致异常造血。通过RNA-seq可以在小鼠成红细胞系中检测到MIWI 2 mRNA，并且该mRNA的shRNA介导的敲低导致细胞呈现分化的红细胞前体的特征。然而，在MIWI 2缺陷小鼠模型中没有可检测到的造血异常。虽然与野生型小鼠相比，在没有功能性MIWI 2基因的小鼠的造血功能中注意到细微的、非统计学显著的变化，但我们的结果表明，MIWI 2不仅仅是小鼠正常寿命内造血所必需的。
Piwi proteins and their small non-coding RNA partners are involved in the maintenance of stem cell character and genome integrity in the male germ cells of mammals. MIWI2, one of the mouse Piwi-like proteins, is expressed in the prepachytene phase of spermatogenesis during the period of de novo methylation. Absence of this protein leads to meiotic defects and a progressive loss of germ cells. There is an accumulation of evidence that Piwi proteins may be active in hematopoietic tissues. Thus, MIWI2 may have a role in hematopoietic stem and/or progenitor cell self-renewal and differentiation, and defects in MIWI2 may lead to abnormal hematopoiesis. MIWI2 mRNA can be detected in a mouse erythroblast cell line by RNA-seq, and shRNA-mediated knockdown of this mRNA causes the cells to take on characteristics of differentiated erythroid precursors. However, there are no detectable hematopoietic abnormalities in a MIWI2-deficient mouse model. While subtle, non-statistically significant changes were noted in the hematopoietic function of mice without a functional MIWI2 gene when compared to wild type mice, our results show that MIWI2 is not solely necessary for hematopoiesis within the normal life span of a mouse.
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影响因子：
14.9
作者：
Meyer LR;Zweig AS;Hinrichs AS;Karolchik D;Kuhn RM;Wong M;Sloan CA;Rosenbloom KR;Roe G;Rhead B;Raney BJ;Pohl A;Malladi VS;Li CH;Lee BT;Learned K;Kirkup V;Hsu F;Heitner S;Harte RA;Haeussler M;Guruvadoo L;Goldman M;Giardine BM;Fujita PA;Dreszer TR;Diekhans M;Cline MS;Clawson H;Barber GP;Haussler D;Kent WJ
通讯作者：
Kent WJ
影响因子：
2.6
作者：
Kuramochi-Miyagawa, S;Kimura, T;Nakano, T
通讯作者：
Nakano, T
影响因子：
20.3
作者：
Sharma, AK;Nelson, MC;Hoffman, R
通讯作者：
Hoffman, R
影响因子：
16
作者：
Aravin, Alexei A.;Sachidanandam, Ravi;Bourc'his, Deborah;Schaefer, Christopher;Pezic, Dubravka;Toth, Katalin Fejes;Bestor, Timothy;Hannon, Gregory J.
通讯作者：
Hannon, Gregory J.
DOI：
10.4049/jimmunol.1000855
发表时间：
2010-08-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Cichocki F;Lenvik T;Sharma N;Yun G;Anderson SK;Miller JS
通讯作者：
Miller JS