1. The Long Noncoding RNA SPRIGHTLY Regulates Cell Proliferation in Primary Human Melanocytes 
Wei Zhao, Joseph Mazar, Bongyong Lee, Junko Sawada, Jian-Liang Li, John Shelley, Subramaniam Govindarajan, Dwight Towler, John S. Mattick, Masanobu Komatsu, Marcel E. Dinger, Ranjan J. Perera 
Journal of Investigative Dermatology 
Volume 136, Issue 4, Pages (April 2016)
DOI: /j.jid
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2. Figure 1
Morphological and gene ontology changes in melanocytes that ectopically express SPRIGHTLY. (a) Melanocytes ectopically expressing SPRIGHTLY (melanocyte SPRIGHTLY-EE) show a multinucleated and multidendritic-like phenotype. (b) Gene ontology and KEGG pathway enrichments determined from genes significantly differentially expressed between SPRIGHTLY-EE melanocytes compared to vector-only control melanocytes by RNA sequencing. P < Bar = 10 μm.
Journal of Investigative Dermatology  , DOI: ( /j.jid )
Copyright © 2016 The Authors Terms and Conditions

3. Figure 2
Gene ontology (GO) enrichment. Statistically significant and differentially expressed genes were used for GO enrichment (SPRIGHTLY-EE vs melanocyte vector-only [VO]). GoGraphViz (Principe Felipe Research Center, Valencia, Spain) visualizations show (a) biological process, (b) cellular component, and (c) molecular function GO terms. Adjusted P < for GO terms were considered significant. The GO enrichments and visualizations were performed using Babelomics 4.3 (Principe Felipe Research Center) (Medina et al., 2010).
Journal of Investigative Dermatology  , DOI: ( /j.jid )
Copyright © 2016 The Authors Terms and Conditions

4. Figure 3
Differentially expressed proliferation, cell cycle, and apoptosis-related genes in SPRIGHTLY-EE cells compared to melanocyte vector-only. Relative expression of CDK1, CDC20, MCM2, MCM3, MCM4, MCM5, Ki-67, and TNFRSF25 in SPRIGHTLY-EE versus melanocyte vector-only.
Journal of Investigative Dermatology  , DOI: ( /j.jid )
Copyright © 2016 The Authors Terms and Conditions

5. Figure 4
MCM2 knockdown on cell viability, growth, and invasiveness. A375 cells transfected with an MCM2-specific small interfering RNA (siRNA) and compared to scramble control siRNA. (a) Quantitative reverse transcriptase-PCR demonstrates the effect of MCM2-specific knockdown relative to scrambled control. (b) Immunohistochemistry staining of A375 cells using MCM2-specific antibodies. MCM2 staining shown in yellow (fluorescein isothiocyanate) and nuclei in blue (4',6-diamidino-2-phenylindole). Bar = 200 μm. (c) Knockdown of MCM2 affects A375 cell viability (CellTiter 96 AQueous). (d) Knockdown of MCM2 affects A375 cell number. (e) Knockdown of MCM2 suppresses A375 invasion. (f) Staining of A375 cells (crystal violet) 48 hours after transfection with MCM2 siRNA reveals a decrease in cell invasion. All results are expressed as mean ± standard deviation of three experiments. Bar = 200 μm. Data for (a) and (e) were normalized to the scramble-transfected control.
Journal of Investigative Dermatology  , DOI: ( /j.jid )
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6. Figure 5
Ki-67 and dipeptidyl peptidase-IV (DPPIV) expression in melanocytes ectopically expressing SPRIGHTLY. (a) Immunofluorescence staining of Ki-67 in SPRIGHTLY-EE, vector-only melanocytes, and A375 cells. Ki-67 nuclear staining is highest in A375 cells. Ki-67 staining is elevated in SPRIGHTLY-EE cells compared to vector-only controls. Bar = 80 μm. (b) Immunofluorescence staining of DPPIV in SPRIGHTLY-EE cells, vector-only melanocytes, and A375 cells. Control melanocytes display abundant cell-surface DPPIV, A375 cells express little or no DPPIV, and SPRIGHTLY-EE cells show intermediate expression levels, that is, an inverse pattern to Ki-67. Bar = 20 μm. (c) DPPIV protein levels (western blot) in SPRIGHTLY-EE cells relative to melanocytes alone and melanocytes transfected with empty vector. (d) Ectopic expression of SPRIGHTLY down-regulates DPPIV mRNA levels in melanocytes. (e) Small interfering RNA-mediated knockdown of SPRIGHTLY up-regulates DPPIV mRNA levels in A375 melanoma cells. Ab, antibody; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.
Journal of Investigative Dermatology  , DOI: ( /j.jid )
Copyright © 2016 The Authors Terms and Conditions