From the speaker: "The application of cultivation independent genomics-based methods to human and animal microbiomes has uncovered bacteria from lineages not represented in culture collections and provided clues as to their metabolic capacities. There is now sufficient genomic sampling to begin to ask questions about how often bacteria from these groups migrate from the natural environment into human microbiomes, from where, what is involved in habitat transition and when metabolic changes occurred.
African genomes harbor millions of uncaptured variants accumulated over 300,000 years of modern humans' evolutionary history, with successive waves of admixture, migration, and natural selection combining with extensive ecological diversity to create a broad and exceptional genomic complexity. Therefore to embrace the prospects of accurately diagnosing thousands of monogenic conditions, predicting disease risks for complex traits or diseases, tailoring treatment to individuals' pharmacogenetic profiles, and potentially curing some diseases, research into African genomic variation is a scien
The ability to maintain a functional proteome by preserving protein homeostasis or proteostasis is essential for cell viability. Yet, this ability declines during the process of aging. Such a collapse in proteostasis results in the accumulation of misfolded and aggregated proteins that are a hallmark of aging and neurodegenerative diseases such as Huntington’s and Alzheimers Disease. Our work aims to define fundamental principles of protein folding and quality control and to apply this knowledge to proteostasis dysfunction in disease.
Regulation of gene expression is crucial for every function carried out by the cell, from cell growth and proliferation to the ability of the cell to respond to its ever-changing environment. Hence, understanding cellular function and dysfunction is dependent upon deciphering these gene regulatory mechanisms. This is particularly challenging in the case of eukaryotic genes, which are often interrupted by long stretches of noncoding sequences (introns). These are removed from the newly synthesized RNA, and the remaining sequences (exons) are ligated together to form a mature messenger RNA.
Dr. Germain will describe the critical role of imaging in developing a deep understanding of how the innate and adaptive immune systems operate in health and disease. He will provide examples of how dynamic intravital imaging has revealed basic information about cell migration and interactions within lymphoid and non-lymphoid tissues and how this method discovered a previously unknown role of tissue resident macrophages in preventing persistent tissue damage by neutrophil ‘swarms’.
Leslie Vosshall wants to understand how environmental cues and internal physiology work together to guide complex animal behaviors. Vosshall and her team study this problem in mosquitoes and humans, applying approaches in neurobiology, behavior, genetics, and genomics. Vosshall’s team uses CRISPR/Cas9 genome-editing tools to advance understanding of how the mosquitoes that spread dengue and yellow fever integrate sensory cues to hunt their human hosts.
Steve Holland's research entails immune defects of phagocytes: GATA2 deficiency (MonoMAC), nontuberculous mycobacterial infections, chronic granulomatous disease, hyper IgE (Job’s) syndrome, leukocyte adhesion deficiency; cytokines and their receptors in the pathogenesis and therapy of infections; susceptibility to disseminated mycobacterial infections, such as GATA2, autoantibodies to interferon gamma and defects in the interferon gamma/IL-12 pathway; mechanisms of mycobacterial pathogenesis; mechanisms of bacterial pathogenesis (e.g., Burkholderia); mechanisms of Coccidioides
to Iqbal Hamza, Ph.D., University of Maryland School of Medicine
Lecture Summary: "Our long-term objectives are to identify the genes and pathways responsible for heme transport and trafficking in eukaryotes that have remained poorly understood. Many have a preconceived notion that the bulk of heme biology is well-understood. How does heme, a cytotoxic hydrophobic ring with an iron atom, moves within and between cells? How does heme traffic across cellular membranes and get into hemoglobin? These open questions are enormous holes in our knowledge.
NEW TIME AND PLACE: 3 P.M. IN WILSON HALL, BUILDING 1 — Mutation of the p53 gene is a critical event in the elaboration of many tumors of diverse origin. The p53 protein is activated in response to DNA damage, serving as a checkpoint in the elimination or repair of cells with damaged DNA. Alterations in components of the p53 pathway, such as amplification of the Mdm2 gene, which encodes a p53 inhibitor, also contribute to tumorigenesis.
This page was last updated on Thursday, September 1, 2022