Dr. Matthew Church
Associate Professor, University of Montana, Flathead Lake Biological Station
Lab Website | Abstract
Eddy-driven variability in nitrification in the subtropical North Pacific Ocean
Tuesday, September 3
12 PM
AHF 153 (Torrey Webb Room)
Abstract: Nitrification is a key step in the marine nitrogen cycle, controlling oxidation of reduced nitrogen in the ocean. Mesoscale eddies, which vertically perturb isopycnal surfaces within the main pycnocline, are thought to play important roles in upper ocean biogeochemical processes; however, potential impacts of eddies on microbial nitrogen cycling in the dimly-lit mesopelagic waters remains largely unknown. In this talk I will summarize on-going work examining how eddies influence the export of particulate nitrogen (PN), rates of nitrification, and the abundances and spatial distributions of nitrifying Archaea (using the ammonia-monooxygenase gene [amoA] as a biomarker) in the oligotrophic waters of the North Pacific Ocean. Eddies influence upper ocean nutrient pools and fluxes, shape the distributions of nitrifying microorganisms and rates of nitrification in the mesopelagic waters. These results suggest that eddy-mediated changes to the upper ocean can have important roles in modifying nitrogen transformation in the interior waters of the ocean.
Tuesday, September 3, 2019
QCB Colloquium | Dr. Hannah Carter
Dr. Hannah Carter
Assistant Professor, UCSD, Health Sciences
Lab Website
MHC genotype shapes the oncogenic landscape
Thursday, September 5
2 PM
RRI 101
Abstract: Significant insights into tumorigenesis have been gained by characterizing the extensive somatic alterations that arise during cancer and uncovering rare inherited mutations that lead to early onset cancer syndromes. However, little is understood about the role of genetic background in ‘sporadic’ adulthood cancers. Mounting evidence suggests that the somatic evolution of a tumor is influenced by inherited polymorphisms. We investigated this phenomenon in the context of the immune system, which is a major source of selective pressure during tumor development. The genomic region encoding the Major Histocompatibility Complex Class (MHC) is one of the most variable regions in the human population. MHC molecules expose peptide fragments on the cell surface, allowing T-Cell elimination of cells contaminated by foreign peptide. Although this system has evolved as a defense against microbial and viral agents, MHC can also trigger elimination of cells harboring mutant peptides (neoantigens) in cancer. Each individual carries multiple MHC alleles that define the set of peptides that can be effectively presented for immune surveillance. We hypothesized that individual variation in MHC could create personal gaps in immune surveillance, generating individual-specific susceptibility for cells to acquire specific oncogenic mutations. To test this hypothesis, we developed residue-centric patient presentation scores for MHC class I and II molecules and applied them to 1,018 recurrent oncogenic mutations in 9,176 cancer patients. This analysis uncovered a clear signature of immune selection acting on tumors with implications for age at diagnosis, driver occurrence in tumors and frequency of driver mutations in cancer cohorts. Thus, the landscape of oncogenic mutations observed in clinically diagnosed tumors is shaped by MHC genotype-restricted immunoediting during tumor formation, and individual MHC genotype provides information about the mutations likely to emerge in tumors that develop later in life.
Host: Dr. Michael Waterman
Assistant Professor, UCSD, Health Sciences
Lab Website
MHC genotype shapes the oncogenic landscape
Thursday, September 5
2 PM
RRI 101
Abstract: Significant insights into tumorigenesis have been gained by characterizing the extensive somatic alterations that arise during cancer and uncovering rare inherited mutations that lead to early onset cancer syndromes. However, little is understood about the role of genetic background in ‘sporadic’ adulthood cancers. Mounting evidence suggests that the somatic evolution of a tumor is influenced by inherited polymorphisms. We investigated this phenomenon in the context of the immune system, which is a major source of selective pressure during tumor development. The genomic region encoding the Major Histocompatibility Complex Class (MHC) is one of the most variable regions in the human population. MHC molecules expose peptide fragments on the cell surface, allowing T-Cell elimination of cells contaminated by foreign peptide. Although this system has evolved as a defense against microbial and viral agents, MHC can also trigger elimination of cells harboring mutant peptides (neoantigens) in cancer. Each individual carries multiple MHC alleles that define the set of peptides that can be effectively presented for immune surveillance. We hypothesized that individual variation in MHC could create personal gaps in immune surveillance, generating individual-specific susceptibility for cells to acquire specific oncogenic mutations. To test this hypothesis, we developed residue-centric patient presentation scores for MHC class I and II molecules and applied them to 1,018 recurrent oncogenic mutations in 9,176 cancer patients. This analysis uncovered a clear signature of immune selection acting on tumors with implications for age at diagnosis, driver occurrence in tumors and frequency of driver mutations in cancer cohorts. Thus, the landscape of oncogenic mutations observed in clinically diagnosed tumors is shaped by MHC genotype-restricted immunoediting during tumor formation, and individual MHC genotype provides information about the mutations likely to emerge in tumors that develop later in life.
Host: Dr. Michael Waterman
Monday, August 26, 2019
Lab Research Assistant Position Available
I have a Laboratory Research Assistant position open in my lab. Apply if you might have an interest in working with us on our vaginal microbiome projects. We can adjust the position to a wide variety of experience and training.
LINK to apply is online: https://umb.taleo.net/careersection/jobdetail.ftl?job=1900013V&lang=en
Please feel free to contact me directly if you have any questions.
Thanks!
LINK to apply is online: https://umb.taleo.net/careersection/jobdetail.ftl?job=1900013V&lang=en
Please feel free to contact me directly if you have any questions.
Thanks!
Rebecca M. Brotman, PhD, MPH
Associate Professor
Department of Epidemiology and Public Health
Institute for Genome Sciences
University of Maryland School of Medicine
670 West Baltimore Street, Room #3175
Baltimore, MD 21201
phone: (410) 706-6767
fax: (410) 706-1482
email: rbrotman@som.umaryland.edu
Sunday, August 25, 2019
MEB Seminar | Dr. Sheila Kitchen
Dr. Sheila Kitchen
Post-Doc, California Institute of Technology, PI: Dr. Joseph Parker
Research Website
Adaptive potential and limits in Caribbean acroporid corals
Tuesday, August 27
12 PM
AHF 153 (Torrey Webb Room)
Abstract: Reef-building corals are currently threatened by rapid changes in local and global stressors, and hybridization offers a potential shortcut for rapid adaptation and evolutionary rescue in these species. The sympatric corals Acropora palmata and A. cervicornis form the hybrid, A. prolifera, whose abundance has continued to increase while the parental species decline. Previous work indicates that weakened prezygotic isolation mechanisms in A. cervicornis but not A. palmata could allow for continuous unidirectional gene flow between the two species. Furthermore, asymmetric introgression from A. palmata to A. cervicornis has been recorded in three nuclear loci. In contrast, we found evidence for bidirectional introgession across three hybrid zones, although the frequency of hybrids and backcrosses differs across the range. Genome assemblies of A. palmataand A. cervicornis were compared to other corals to identify orthologs uniquely shared by the Caribbean acroporids. Genomic sequence data from the two parental species and their hybrids was used to further characterize the patterns of genomic synteny, divergence and introgression across hybrid zones. Combined, these approaches elucidate genomic hotspots of introgression and parallel evolution with implications for how hybridization may shape adaptation in these important foundation species across the Caribbean and North-West Atlantic.
Host: Dr. Carly Kenkel
Post-Doc, California Institute of Technology, PI: Dr. Joseph Parker
Research Website
Adaptive potential and limits in Caribbean acroporid corals
Tuesday, August 27
12 PM
AHF 153 (Torrey Webb Room)
Abstract: Reef-building corals are currently threatened by rapid changes in local and global stressors, and hybridization offers a potential shortcut for rapid adaptation and evolutionary rescue in these species. The sympatric corals Acropora palmata and A. cervicornis form the hybrid, A. prolifera, whose abundance has continued to increase while the parental species decline. Previous work indicates that weakened prezygotic isolation mechanisms in A. cervicornis but not A. palmata could allow for continuous unidirectional gene flow between the two species. Furthermore, asymmetric introgression from A. palmata to A. cervicornis has been recorded in three nuclear loci. In contrast, we found evidence for bidirectional introgession across three hybrid zones, although the frequency of hybrids and backcrosses differs across the range. Genome assemblies of A. palmataand A. cervicornis were compared to other corals to identify orthologs uniquely shared by the Caribbean acroporids. Genomic sequence data from the two parental species and their hybrids was used to further characterize the patterns of genomic synteny, divergence and introgression across hybrid zones. Combined, these approaches elucidate genomic hotspots of introgression and parallel evolution with implications for how hybridization may shape adaptation in these important foundation species across the Caribbean and North-West Atlantic.
Host: Dr. Carly Kenkel
QCB Colloquium | Dr. Charleston Chiang
Dr. Charleston Chiang
Assistant Professor, USC Keck School of Medicine, Center for Genetic Epidemiology, Preventive Medicine
Lab Website
The impact of demographic history and natural selection on human complex traits: examples from Sardinia and Finland
Thursday, August 29, 2019
2 PM
RRI 101
Abstract: How complex traits change through time is a central question in evolutionary biology and genetics. Two of the major evolutionary forces that shaped the distribution of human complex traits are the demographic and adaptive histories of a population. Therefore, in order for human genetics to provide a compelling context to study complex trait evolution, it is necessary to integrate genetic mapping with a detailed knowledge of population history. A well-known example of demographic impact on complex traits is a population bottleneck followed by long-term isolations. I will use examples from European populations of Sardinia and Finland to illustrate the impact of the demographic history on patterns of genetic variation and human complex traits. By utilizing large-scale whole-genome or whole-exome sequencing datasets, I will describe our findings in delineating the population structure and history of these populations, and how the special population history empowered association studies. Moreover, natural selection through polygenic adaptation is also thought to be an important force in shaping the complex traits of extant populations. Adult height differences across European populations had been thought of as the prime example of polygenic adaptation in humans, until recent papers demonstrated that the differences across Europe might have been over-estimated due to uncorrected biases in genome-wide association studies (GWAS). I will show that by using GWAS summary statistics ascertained from an East Asian population, we continue to see signature consistent with polygenic adaptation at height-associated loci in at least some European populations.
Host: Andrew Smith
Assistant Professor, USC Keck School of Medicine, Center for Genetic Epidemiology, Preventive Medicine
Lab Website
The impact of demographic history and natural selection on human complex traits: examples from Sardinia and Finland
Thursday, August 29, 2019
2 PM
RRI 101
Abstract: How complex traits change through time is a central question in evolutionary biology and genetics. Two of the major evolutionary forces that shaped the distribution of human complex traits are the demographic and adaptive histories of a population. Therefore, in order for human genetics to provide a compelling context to study complex trait evolution, it is necessary to integrate genetic mapping with a detailed knowledge of population history. A well-known example of demographic impact on complex traits is a population bottleneck followed by long-term isolations. I will use examples from European populations of Sardinia and Finland to illustrate the impact of the demographic history on patterns of genetic variation and human complex traits. By utilizing large-scale whole-genome or whole-exome sequencing datasets, I will describe our findings in delineating the population structure and history of these populations, and how the special population history empowered association studies. Moreover, natural selection through polygenic adaptation is also thought to be an important force in shaping the complex traits of extant populations. Adult height differences across European populations had been thought of as the prime example of polygenic adaptation in humans, until recent papers demonstrated that the differences across Europe might have been over-estimated due to uncorrected biases in genome-wide association studies (GWAS). I will show that by using GWAS summary statistics ascertained from an East Asian population, we continue to see signature consistent with polygenic adaptation at height-associated loci in at least some European populations.
Host: Andrew Smith
Monday, May 6, 2019
Post-Doc @ Univ. of Maryland School of Medicine
A postdoctoral position is available in the laboratory of Dr. David Serre at the Institute for Genome Sciences at the University of Maryland School of Medicine. Our laboratory is interested in developing and applying novel genomic approaches to better understand the biology of malaria parasites and the vectors that transmit them.
We are seeking a highly motivated individual to take the lead on analyses of single-cell RNA-seq data generated from Plasmodiumparasites at different life stages of their development and under various conditions. This postdoctoral position is supported by NIH awards and involves collaborations with researchers at NIAID, Johns Hopkins School of Public Health and in malaria-endemic countries. There are also opportunities for the successful candidate to develop her/his own independent projects within the framework of this research.
A PhD in biology, bioinformatics, genomics or a related field is required. The work involves custom bioinformatic analyses of large amount of data and proficiency in one programming language and knowledge of statistics would be an advantage. Previous knowledge of parasitology is not required.
Interested candidates should send a cover letter and CV to David Serre (dserre@som.umaryland.edu)
We are seeking a highly motivated individual to take the lead on analyses of single-cell RNA-seq data generated from Plasmodiumparasites at different life stages of their development and under various conditions. This postdoctoral position is supported by NIH awards and involves collaborations with researchers at NIAID, Johns Hopkins School of Public Health and in malaria-endemic countries. There are also opportunities for the successful candidate to develop her/his own independent projects within the framework of this research.
A PhD in biology, bioinformatics, genomics or a related field is required. The work involves custom bioinformatic analyses of large amount of data and proficiency in one programming language and knowledge of statistics would be an advantage. Previous knowledge of parasitology is not required.
Interested candidates should send a cover letter and CV to David Serre (dserre@som.umaryland.edu)
QCB Colloquium Series | Dr. Hongyu Zhao
Dr. Hongyu Zhao
Department Chair and Ira V. Hiscock Professor of Biostatistics, Professor of Genetics and Professor of Statistics and Data Science, Yale University, School of Public Health
Lab Website
Dissecting Genetic Architecture of Complex Diseases From Genome Wide Association Studies
Wednesday, May 8, 2019
2 PM
RRI 301
Abstract: Genome-wide association study (GWAS) has been a great success in the past decade, with thousands of regions in the human genome implicated for hundreds of complex diseases. However, significant challenges remain in both identifying new risk loci and interpreting results, even for samples with tens of thousands of subjects. In this presentation, we describe our recent efforts to infer the genetic architecture of complex disease through random effects models, the development of functional annotations of the human genome, and the integrated analysis of these annotations with GWAS results. The effectiveness of our methods will be demonstrated through their applications to a large number of GWASs to identify tissues/cell types that are relevant to a specific disease, to infer shared genetic contributions to several diseases, and to improve genetic disease risk predictions. This is joint work with Qiongshi Lu, Yiming Hu, Jiming Jiang, Can Yang, Ryan Powels, Yixuan Ye, and others.
Department Chair and Ira V. Hiscock Professor of Biostatistics, Professor of Genetics and Professor of Statistics and Data Science, Yale University, School of Public Health
Lab Website
Dissecting Genetic Architecture of Complex Diseases From Genome Wide Association Studies
Wednesday, May 8, 2019
2 PM
RRI 301
Abstract: Genome-wide association study (GWAS) has been a great success in the past decade, with thousands of regions in the human genome implicated for hundreds of complex diseases. However, significant challenges remain in both identifying new risk loci and interpreting results, even for samples with tens of thousands of subjects. In this presentation, we describe our recent efforts to infer the genetic architecture of complex disease through random effects models, the development of functional annotations of the human genome, and the integrated analysis of these annotations with GWAS results. The effectiveness of our methods will be demonstrated through their applications to a large number of GWASs to identify tissues/cell types that are relevant to a specific disease, to infer shared genetic contributions to several diseases, and to improve genetic disease risk predictions. This is joint work with Qiongshi Lu, Yiming Hu, Jiming Jiang, Can Yang, Ryan Powels, Yixuan Ye, and others.
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