We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Deficiency of MIWI2 (Piwil4) Induces Mouse Erythroleukemia Cell Differentiation, but Has No Effect on Hematopoiesis <i>In Vivo</i>.
- Authors
Jacobs, James E.; Wagner, Mark; Dhahbi, Joseph; Boffelli, Dario; Martin, David I. K.
- Abstract
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.
- Subjects
ACUTE erythroid leukemia; CANCER cell differentiation; HEMATOPOIESIS; PIWI genes; NON-coding RNA; GERM cells; LABORATORY mice
- Publication
PLoS ONE, 2013, Vol 8, Issue 12, p1
- ISSN
1932-6203
- Publication type
Article
- DOI
10.1371/journal.pone.0082573