Primary Faculty


Bassem Al-Sady, PhD
Associate Professor, Department of Microbiology & Immunology, The George William Hooper Foundation

  "Mechanisms of Formation and Maintenance of Epigenetic Elements"

Dr. Al-Sady's research interests reside in uncovering the mechanisms that underlie the assembly and fidelity of inheritance of heterochromatin, a specialized protein-nucleic acid composite. Unraveling these mechanisms is key to understanding the manner in which large stretches of the genome can be precisely and heritably partitioned into active and inactive regions. The heterochromatin system presents some unique and unusual features for a cellular self-assembly, such as nucleated, template-guided polymerization to a precise positional extent that have remained difficult to study. Addressing these features requires a multidisciplinary framework integrating biochemical and novel single cell genetic approaches. 

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Raul Andino, PhD
Professor, Department of Microbiology & Immunology

"Replication of RNA Viruses and Vaccine Development" 

Dr. Andino studies several processes of the replication cycle of RNA viruses, including the mechanism of RNA replication, expression, and RNA packaging. His lab has also developed a method of adapting positive-stranded RNA as a vaccine vector to express antigenic determinants derived from diverse pathogens.

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K. Mark Ansel, PhD
Professor, Department of Microbiology & Immunology

"Molecular Mechanisms of Gene Regulation in T lymphocytes"

Dr. Ansel studies molecular mechanisms of gene regulation in T lymphocytes. Transcription factors, chromatin remodeling, and microRNAs all contribute to the gene expression prorams that underlie the development of the different types of effector T cells that direct appropriate immune responses against differerent types of pathogens. 

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Joe Bondy-Denomy, PhD
Associate Professor, Department of Microbiology & Immunology

Dr. Bondy-Denomy is interested in elucidating the molecular strategies deployed by bacterial viruses (phages) when they infect their host. Bacteria face a constant threat of phage infection, which has driven the evolution of numerous anti-phage immune systems, including restriction enzymes and CRISPR-Cas systems. The Bondy-Denomy lab uses a combination of genetic, molecular and biochemical approaches to discover and characterize the factors that control this arms race, striving to better understand microbial ecosystems and develop better treatments for bacterial pathogens.

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Jason Cyster, PhD
Professor and Vice Chair, Department of Microbiology & Immunology

Investigator, Howard Hughes Medical Institute 

"Molecular Regulation of Cell Migration and Survival in Lymphoid Tissues"

Dr. Cyster is focused on defining the molecular cues that guide leukocyte migration in secondary lymphoid organs, and on determining how cell position influences cell fate. These investigations have implications for understanding how immune function and self-tolerance are maintained in healthy individuals, and how these processes break down in states of autoimmunity or hematopoietic malignancy.

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Tony DeFranco, PhD
Professor, Department of Microbiology & Immunology

The DeFranco lab studies signal transduction by the B cell antigen receptor (BCR) and by Toll-like receptors (TLRs) and is particularly interested in how signaling supports the proper functioning of the immune system.  They are also interested in how alterations in these signaling pathways may lead to disease.

BCR signaling involves activation of intracellular protein tyrosine kinases of three types and downstream activation of a variety of signaling reactions.  Although Src-family tyrosine kinases play a very important role in the initiation of signaling, B cells express three family members and one of these, Lyn, also is important for feedback inhibition of BCR signaling.  In the absence of Lyn, BCR signaling proceeds with a slight delay, but feedback inhibition is defective, resulting in exaggerated signaling and spontaneous autoimmune disease that resembles the human disease systemic lupus erythrematosus.  A major project in the lab involves studying how deficiency in Lyn leads to defects in B cell tolerance and spontaneous autoimmune disease.  These studies are part of a long-term collaboration with Clifford Lowell, who studies the function of Lyn in myeloid cells and how alterations in myeloid cells also contribute to the autoimmunity observed in the Lyn-/- mice.  A second major project in this area is to understand how BCR signaling is differentially regulated between immature and mature B cells.  Immature B cells are highly sensitive to antigen, leading to tolerance-related responses such as receptor editing and anergy, whereas mature B cells are less sensitive but exhibit robust signaling when the BCR is strongly engaged, a dose response behavior which likely reflects a threshold for activation.  One of the feedback inhibitory pathways controlled by Lyn (involving CD22) is strongly active in mature B cells and less active in immature B cells, but this does not account for all differences in the sensitivity to antigen.  Recently we have begun to analyze how the diacylglycerol kinases may contribute to regulation of the activation of mature B cells. TLR signaling is important for many immune responses and occurs in most if not all immune cell types in response to infections.  For this reason, it has been hard to distinguish the relative contributions of different cell types for TLR-dependent immune reactions.  To address this problem, we have created a conditional allele of the critical TLR signaling component Myd88 in which an essential exon is surrounded by loxP sites.  Cell type-specific expression of the Cre recombinase results in deletion of the Myd88 gene in that cell type.  We have used mice in which Myd88 is deleted to demonstrate that TLR signaling in dendritic cells plays an essential role for the innate immune restriction of growth by the single-celled parasite Toxoplasma gondii.  Similarly, Myd88 in dendritic cells was required for a normal magnitude IgG response to soluble protein antigens covalently coupled to a TLR ligand.  In contrast, Myd88 function in B cells, but not dendritic cells was found to greatly enhance the IgG germinal center response to virus particles.  This may represent an adaptation of the immune system designed to boost antibody responses to virus particles. These studies illustrate that TLR signaling is important for many immune responses and begin to define how this occurs in vivo.


Carol Gross, PhD
Professor and Vice Chair, Depts. of Microbiology & Immunology, Cell & Tissue Biology 

"Regulation of Gene Expression"

Dr. Gross works on the regulation of the E. coli stress response, protein interactions in the bacterial transcription apparatus, and genomic analysis of gene expression using E. coli microarrays.

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Alexander (Sandy) Johnson, PhD
Professor and Vice Chair, Depts. of Microbiology & Immunology, Biochemistry & Biophysics

"Control of Gene Expression"

Dr. Johnson studies several basic problems in transcriptional regulation using the model yeast Saccharomyces cerevisiae. His laboratory also studies several features of the human opportunistic pathogen Candida albicans and the relationships of these features to its virulence.

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Lewis Lanier, PhD
Professor, Chair, Department of Microbiology and Immunology, The George William Hooper Foundation
Director, Parker Institute for Cancer Immunotherapy

"Regulation of T-cell and NK-cell Immune Responses by Activating and Inhibitory Receptors"

Dr. Lanier has focused on membrane receptors on T cells and NK cells that recognize classical and non-classical major histocompatibility complex (MHC) antigens. A major focus of the Lanier lab is to determine the ligand specificity of these receptors, their signal transduction pathways, and their physiological relevance in immune responses against tumors and pathogens.

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Joachim Li, MD, PhD
Professor, Department of Microbiology & Immunology

"Regulation of Eukaryotic DNA Replication"

Dr. Li is interested in understanding the control of eukaryotic DNA replication during the cell cycle and the genetic consequences of disrupting that control. He is studying this problem in the yeast Saccharomyces cerevisiae.




Michael McManus, PhD
Director, UCSF Keck Center for Noncoding RNAs

Director, UCSF Sandler Lentiviral RNAi Core
Professor, Department of Microbiology and Immunology
UCSF Diabetes Center 

The "Dark Matter" of our genome constitutes the vast spaces between the genes that encode for proteins- it was once mistakenly thought as being "junk DNA." The McManus lab now knows that these seemingly empty spaces contain thousands of hidden genes, most of which do not appear to make proteins, but instead noncoding RNAs of unknown function. The lab is focused on this exciting class of genes, with the hope of better illuminating its functions and mechanisms in eukaryotic gene regulation- and its relationship to human disease. The McManus lab has developed cutting-edge research tools- employing high-throughput genome-wide RNAi screens, deep sequencing, and even mouse models to establish the biological importance of this Dark Matter substance.

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Shaeri Mukherjee, PhD
Associate Professor, Department of Microbiology & Immunology, The George William Hooper Foundation

"Turning pathogens into cell biology tools"

Dr. Mukherjee is interested in elucidating how intracellular bacterial pathogens subvert host cell endocytic and secretory pathways to create a replicative niche for themselves.

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Suzanne Noble, MD, PhD
Associate Professor, Department of Microbiology & Immunology and Department of Medicine, Division of Infectious Diseases

"Commensalism and Pathogenesis of the Yeast, Candida albicans"

Candida albicans is an unusual fungal member of the human microbiome and the most common cause of human fungal infections. The Noble laboratory uses an array of powerful approaches to dissect the interactions betweenC. albicans, commensal bacteria, and the mammalian host to understand in precise molecular terms its remarkable ability to transition between programs of commensalism and virulence.

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Karin Pelka, PhD
Assistant Professor, Department of Microbiology and Immunology, Gladstone Institutes​


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Angela Phillips, Ph.D
Assistant Professor, Department of Microbiology & Immunology

The Phillips lab is interested in elucidating the molecular mechanisms that constrain protein evolution at the host-virus interface. The lab develops high-throughput methods to evolve, mutagenize, and biophysically characterize viral proteins and antibodies to better understand the properties that shape their evolution and co-evolution. 


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(Scott Eisen/HHMI)


Kole Roybal, Ph.D
Associate Professor, Department of Microbiology & Immunology, Parker Institute for Cancer Immunotherapy

“Engineering Immune Cells to Expand their Therapeutic Potential”

The Roybal lab harnesses the tools of synthetic and chemical biology to engineer immune cells for cancer immunotherapy. We take a comprehensive approach to cellular engineering by developing new synthetic receptors, signal transduction cascades, and cellular response programs to enhance the safety and effectiveness of adoptive cell therapies. We also study the logic of natural cellular signaling systems, and the underlying principles of cellular communication and collective cell behavior during an immune response. These interests are complimentary as cell engineering is often informed by knowledge obtained from studying natural mechanisms of cell regulation refined by evolution.

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Anita Sil, MD, PhD
Professor and Vice Chair, Department of Microbiology & Immunology

"Fungal Pathogenesis and Host Response"

Dr. Sil studies the human pathogen Histoplasma capsulatum, delving into the cell biology of both the microbe and the relevant host cells. The goal of her research is to use functional genomics and genetics to generate a molecular understanding of how cell-cell interaction, signal transduction, gene regulation, and other fundamental biological processes influence pathogenesis.

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Peter Turnbaugh, PhD
Professor, Department of Microbiology & Immunology,
The George William Hooper Foundation

'The Gut Microbiome, Pharmacology, and Nutrition'The microbes residing in and on the human body influence host health and disease in part due to their metabolism of xenobiotics (foreign compounds like host-targeted drugs, antibiotics, and dietary components). Yet microbial xenobiotic metabolism remains an underexplored aspect of pharmacology and nutrition, with the bacterial groups and metabolic pathways responsible often unknown. We are addressing this critical knowledge gap through the use of methods for the single cell analysis of gut microbial communities, metagenomic sequencing of microbial community DNA and RNA, and gnotobiotics (germ-free and colonized mice). Ultimately, we aim to obtain a more comprehensive view of human metabolism, yielding fundamental insights into host-microbial interactions and supporting translational efforts to predict and manipulate the metabolic activities of our resident gut microbes.

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