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. Author manuscript; available in PMC: 2016 Mar 16.
Published in final edited form as: Annu Rev Cell Dev Biol. 2013 Jul 12;29:213–239. doi: 10.1146/annurev-cellbio-101512-122343

Figure 2.

Figure 2

Phenotypes of Dicer and Dgcr8 knockout. (Row 1) Small RNA populations present in each knockout. (Row 2) Effect of maternal or maternal-zygotic deletion of Dicer and Dgcr8 on development. Maternal Dicer knockout oocytes do not complete maturation, whereas maternal-zygotic knockout Dgcr8 oocytes mature and develop to the blastocyst stage. (Row 3) Effect of knockouts on mouse embryonic stem cell (mESC) biology. mESCs lacking Dicer or Dgcr8 retain their ability to self-renew and can initiate differentiation, but they fail to silence pluripotency factors and acquire a delayed G1-to-S transition. (Row 4) Knockout of either Dicer or Dgcr8 in mouse embryonic fibroblasts (MEFs) results in cell cycle arrest and senescence. (Row 5) Cell cycle arrest in Dicer knockout MEFs prevents reprogramming, but Dicer knockout after initiation of reprogramming is permissive for induction of pluripotent stem cells (PSCs). Abbreviations: microRNA, miRNA; siRNA, small interfering RNA.

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