Added citation for newly submitted paper

citations.bib

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-%% Created for Ryan C. Thompson at 2016-09-24 11:12:07 -0700 
+%% Created for Ryan C. Thompson at 2016-10-25 15:10:59 -0700 
 
 
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+@article{lamere2016-JMJD3,
+	Abstract = {The changes to the epigenetic landscape in response to antigen during CD4 T cell activation have not been well characterized. While CD4 T cell subsets have been mapped globally for numerous epigenetic marks, little has been done to study their dynamics early after activation. We have studied changes to promoter H3K27me3 during activation of human na{\"\i}ve and memory CD4 T cells. Our results show that these changes occur relatively early (1 day) after activation of both na{\"\i}ve and memory cells, and that H3K27 demethylation is the predominant change at this time point, reinforcing high expression of target genes. Additionally, we also examined bivalent gene promoters (i.e. those containing both H3K4me3 and H3K27me3) and show that this state is dynamic during activation with different outcomes comparing na{\"\i}ve and memory subsets, despite strong overlap between mapped functional pathways. Additionally, inhibition of the H3K27 demethylase, JMJD3, in na{\"\i}ve CD4 demonstrates how the critical JAK/STAT pathways are regulated during activation by H3K27 demethylation. Our results demonstrate that H3K27me3 is a dynamic and important epigenetic modification during CD4 T cell activation and differentiation, and that JMJD3-driven H3K27 demethylation is integral to CD4 T cell function.},
+	Author = {LaMere, Sarah and \textbf{Ryan C. Thompson} and Meng, Xiangzhi and Komori, H. Kiyomi and Mark, A. and Salomon, Daniel R.},
+	Date-Added = {2016-10-25 21:40:16 +0000},
+	Date-Modified = {2016-10-25 22:04:38 +0000},
+	Journal = {Journal of Experimental Medicine (in review)},
+	Title = {{H3K27} methylation dynamics during {CD4} {T} cell activation: regulation of {JAK}/{STAT} and {IL12RB2} expression by {JMJD3}},
+	Year = {2016}}
+
 @article{lamere2016,
 	Abstract = {The epigenetic determinants driving the responses of CD4 T cells to antigen are currently an area of active research. Much has been done to characterize helper T-cell subsets and their associated genome-wide epigenetic patterns. In contrast, little is known about the dynamics of histone modifications during CD4 T-cell activation and the differential kinetics of these epigenetic marks between naive and memory T cells. In this study, we have detailed the dynamics of genome-wide promoter H3K4me2 and H3K4me3 over a time course during activation of human naive and memory CD4 T cells. Our results demonstrate that changes to H3K4 methylation occur relatively late after activation (5 days) and reinforce activation-induced upregulation of gene expression, affecting multiple pathways important to T-cell activation, differentiation and function. The dynamics and mapped pathways of H3K4 methylation are distinctly different in memory cells, which have substantially more promoters marked by H3K4me3 alone, reinforcing their more differentiated state. Our study provides the first data examining genome-wide histone modification dynamics during CD4 T-cell activation, providing insight into the cross talk between H3K4 methylation and gene expression, and underscoring the impact of these marks upon key pathways integral to CD4 T-cell activation and function.Genes and Immunity advance online publication, 12 May 2016; doi:10.1038/gene.2016.19.},
-	Author = {LaMere, S. A. and \textbf{Ryan C. Thompson} and Komori, H. K. and Mark, A. and Salomon, D. R.},
+	Author = {LaMere, Sarah and \textbf{Ryan C. Thompson} and Komori, H. Kiyomi and Mark, Adam and Salomon, Daniel R.},
 	Date-Added = {2016-06-10 14:29:31 +0000},
-	Date-Modified = {2016-06-10 14:30:40 +0000},
-	Journal = {Genes Immun.},
+	Date-Modified = {2016-10-25 22:10:59 +0000},
+	Journal = {Genes \& Immunity},
 	Month = {May},
 	Title = {{{P}romoter {H}3{K}4 methylation dynamically reinforces activation-induced pathways in human {C}{D}4 {T} cells}},
 	Year = {2016}}
 
 @article{globin-reduction,
-	Abstract = {Primate blood contains high concentrations of globin messenger RNA. Globin reduction is a standard technique used to improve the expression results obtained by DNA microarrays on RNA from blood samples. However, with whole transcriptome RNA-sequencing (RNA-seq) quickly replacing microarrays for many applications, the impact of globin reduction for RNA-seq has not been previously studied. Moreover, no off-the-shelf kits are available for globin reduction in nonhuman primates. Here we report a protocol for RNA-seq in primate blood samples that uses complimentary oligonucleotides to block reverse transcription of the alpha and beta globin genes. In test samples from cynomolgus monkeys (Macaca fascicularis), this globin blocking protocol approximately doubles the yield of informative (non-globin) reads by greatly reducing the fraction of globin reads, while also improving the consistency in sequencing depth between samples. The increased yield enables detection of about 2000 more genes, significantly increases the correlation in measured gene expression levels between samples, and increases the sensitivity of differential gene expression tests. These results show that globin blocking significantly improves the cost-effectiveness of mRNA sequencing in primate blood samples by doubling the yield of useful reads, allowing detection of more genes, and improving the precision of gene expression measurements. Based on these results, a globin reducing or blocking protocol is recommended for all RNA-seq studies of primate blood samples.
},
+	Abstract = {Primate blood contains high concentrations of globin messenger RNA. Globin reduction is a standard technique used to improve the expression results obtained by DNA microarrays on RNA from blood samples. However, with whole transcriptome RNA-sequencing (RNA-seq) quickly replacing microarrays for many applications, the impact of globin reduction for RNA-seq has not been previously studied. Moreover, no off-the-shelf kits are available for globin reduction in nonhuman primates. Here we report a protocol for RNA-seq in primate blood samples that uses complimentary oligonucleotides to block reverse transcription of the alpha and beta globin genes. In test samples from cynomolgus monkeys (Macaca fascicularis), this globin blocking protocol approximately doubles the yield of informative (non-globin) reads by greatly reducing the fraction of globin reads, while also improving the consistency in sequencing depth between samples. The increased yield enables detection of about 2000 more genes, significantly increases the correlation in measured gene expression levels between samples, and increases the sensitivity of differential gene expression tests. These results show that globin blocking significantly improves the cost-effectiveness of mRNA sequencing in primate blood samples by doubling the yield of useful reads, allowing detection of more genes, and improving the precision of gene expression measurements. Based on these results, a globin reducing or blocking protocol is recommended for all RNA-seq studies of primate blood samples.
+},
 	Author = {\textbf{Ryan C. Thompson} and Terri Gelbart and Steven R. Head and Phillip Ordoukhanian and Courtney Mullen and Dongmei Han and Dora M. Berman and Amelia Bartholomew and Norma S. Kenyon and Daniel R. Salomon},
 	Date-Added = {2016-05-03 23:39:31 +0000},
 	Date-Modified = {2016-09-24 18:11:49 +0000},

ryan_thompson_resume.lyx

@@ -218,14 +218,14 @@ Salomon Lab, The Scripps Research Institute
 \end_layout
 
 \begin_layout Itemize
-Created a reproducible workflow to analyze a large multi-omics next-gen
- sequencing dataset of 220 RNA-seq and ChIP-seq samples to reveal interactions
- between differential histone methylation and differential gene expression
- during T-cell activation, as well as key differences in activation between
- naïve and memory cells 
+Created an open source, reproducible workflow to analyze a large multi-omics
+ next-gen sequencing dataset of 220 RNA-seq and ChIP-seq samples to reveal
+ interactions between differential histone methylation and differential
+ gene expression during T-cell activation, as well as key differences in
+ activation between naïve and memory cells 
 \begin_inset CommandInset citation
 LatexCommand cite
-key "lamere2016"
+key "lamere2016,lamere2016-JMJD3"
 
 \end_inset