The Brd2 was also shown to be expressed at high levels in diplotene spermatocytes and round spermatids and at low levels in spermatogonia that negatively co-related with the expression pattern of miR-127. The functions of imprinted miRNAs in testis-derived male germ-line stem cells are not known. They acts in trans, generally outside the genomic region from where they arise, and may even cleave the mRNAs encoded by the same imprinted gene cluster in partner chromosome in a RNAi-like manner. Liu et al., found that imprinted miRNAs encoded by Dlk1-Dio3 locus had 717 putative targets that were related to multiple aspects of growth, differentiation, metabolism and other developmental processes in pluripotent cells. Furthermore, several miRNAs from this cluster potentially target the PRC2 silencing complex to form a feedback regulatory loop resulting in the expression of all genes and Rapamycin 53123-88-9 non-coding RNAs encoded by this locus. On the other hand, Gnas-Nespas cluster encode miR296 and miR-298 which are derived from non-coding Nespas gene transcript. The miR-296 regulates the expression of growth factor receptor in endothelial cells and increases upon in vitro differentiation of ES cells to target the Nanog gene transcript. The Igf2-H19 cluster encodes miR-675 and miR-483 but their precise role in stem cells is not known. An in silico bioinformatic analysis using web-based TargetScan and MicroCosm Targets Version 5 softwares showed that miR-483 has numerous putative targets that included Jarid1b. Jarid1b directly regulates genes that control cancer cell proliferation and may be essential for the stem cell pluripotency. Although Jarid1b is yet to be validated as a target of miR-483, we found that consistent with the high expression of miR-483 in GS cells, the expression of Jarid1b was significantly lower in GS cells than in maGS or ES cells. Moreover, consistent with the expression of Jarid1b, GS cells proliferated slower than maGS cells, as has also been reported earlier. In conclusion, our data suggest that genomic imprinting and expression of imprinted miRNAs are androgenetic in mouse GS cells but changes to ES cell-like pattern upon their conversion to maGS cells. Differential genomic imprinting of imprinted miRNAs may thus serve as epigenetic signature or molecular marker to distinguish GS cells from maGS or ES cells. Since maGS cells originate from GS cells during their extended in vitro culture, our data may have implications in clinical settings to distinguish GS cell colonies from maGS cell colonies and thereby minimize the likelihood of teratoma formation by contaminating maGS cells generated from the GS cells. Conversely, in experimental research settings and regenerative medicine, analysis of imprinted miRNA may help in discriminating maGS cells from GS cells for tissue engineering or studying cellular reprogramming. Prior to clinical and/or research applications.