1. Dissecting the Roles of Polycomb Repressive Complex 2 Subunits in the Control of Skin Development 
Katherine L. Dauber, Carolina N. Perdigoto, Victor J. Valdes, Francis J. Santoriello, Idan Cohen, Elena Ezhkova 
Journal of Investigative Dermatology 
Volume 136, Issue 8, Pages (August 2016)
DOI: /j.jid
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2. Figure 1
Loss of PRC2 leads to premature epidermis formation. (a) Hematoxylin and eosin staining showing similar epidermal structure in P0 WT and PRC2-null mice; quantification of epidermal thickness (n ≥ 2; P = ). (b–d) Immunofluorescence for Krt10 (K10) (b), Loricrin (Lor) (c), and Filaggrin (Flg) (d) showing that the differentiated suprabasal layers are unaffected in P0 PRC2-null mice. (e) Immunofluorescence for BrdU showing no changes in proliferation in the integrin β4 (β4)-labeled basal layer (BL) in P0 PRC2-null mice; quantification of percentage of BrdU(+) cells (n = 3; P = ). (f, g) Hematoxylin and eosin (H&E) staining (f) and immunofluorescence for Filaggrin (g) showing premature formation of the stratum corneum in E16 PRC2-null mice when compared with WT. Scale bars: 25 μm. Statistical significance: non significant (n.s.) P > der, dermis; epi, epidermis; Krt, keratin; PRC2, polycomb repressive complex 2.
Journal of Investigative Dermatology  , DOI: ( /j.jid )
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3. Figure 2
Loss of PRC2 results in Merkel cell expansion. (a) Immunofluorescence for Krt20 (K20) showing a significant increase in the number of Merkel cells (MC) in P0 PRC2-null epidermis, compared with WT; quantification of number of MC (n ≥ 3; P < ). (b, c) Immunofluorescence for MC markers Krt20 (b), Isl1 (b), Krt18 (K18) (c), and Sox2 (c) showing coexpression of markers in PRC2-null MC. (d) Immunofluorescence for Krt20 and NF200 showing that the PRC2-null MC are innervated. (e) Ki67 staining showing that MC are not proliferating in P0 PRC2-null epidermis. (f) RT-qPCR in FACS-purified interfollicular epidermis (IFE) cells showing upregulation of Merkel genes Isl1 and Sox2 in P14 gWT and gPRC-null skin (mean ± SD; n = 3; all significant, P < 0.05). Scale bars: (a) 100 μm; (b–e) 25 μm. Statistical significance: significant *P = 0.01–0.05; very significant **P = 0.01–0.001; extremely significant ***P < FACS, fluorescence-activated cell-sorting; Krt, keratin; PRC2, polycomb repressive complex 2; RT-qPCR, semiquantitative real-time PCR.
Journal of Investigative Dermatology  , DOI: ( /j.jid )
Copyright © 2016 The Authors Terms and Conditions

4. Figure 3
Loss of PRC2 causes reduced proliferation and increased apoptosis in hair follicles. (a) Hematoxylin and eosin showing that P14 gPRC2-null mice have shorter hair follicles (HFs) than gWT; quantification of HF length (n ≥ 2; P < ). (b) BrdU staining showing reduced proliferation in the matrix (Mx) of P14 gPRC2-null HFs; quantification of percentage of BrdU(+) matrix cells (n = 3; gEEDcKO, P = ; gSuz12cKO, P < ). AE13 marks matrix limit. (c) Activated Caspase 3 (Casp3) staining showing increased apoptosis in P14 gPRC2-null HFs, labeled with E-Cadherin (Ecad); quantification of percentage of Casp3(+) HFs (n ≥ 2; gEEDcKO, P = ; gSuz12cKO, P = ). (d) RT-qPCR of FACS-purified outer root sheath (ORS) cells showing p15 (INK4B), p16 (INK4A), and p19 (ARF) upregulation in P14 gPRC2-null mice (mean ± SD; n = 3; all significant, P < 0.05). Scale bars: (a) 100 μm; (b, c) 25 μm. Statistical significance: significant *P = 0.01–0.05; very significant **P = 0.01–0.001; extremely significant ***P < FACS, fluorescence-activated cell-sorting; PRC2, polycomb repressive complex 2; RT-qPCR, semiquantitative real-time PCR; SD, standard deviation.
Journal of Investigative Dermatology  , DOI: ( /j.jid )
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5. Figure 4
Loss of polycomb repressive complex 2 (PRC2) results in three distinct skin phenotypes. Schematic diagram showing how loss of PRC2 affects the development of different skin lineages. Embryonic epidermal progenitors give rise to the epidermis, Merkel cells, and hair follicles. In mice in which either Ezh1/2, EED, or Suz12 are deleted from the epidermal progenitors, there is premature formation of the stratum corneum, an increase in the number of Merkel cells, and defective postnatal hair follicle development due to decreased matrix proliferation and increased apoptosis of the hair follicles.
Journal of Investigative Dermatology  , DOI: ( /j.jid )
Copyright © 2016 The Authors Terms and Conditions