About

Ted Powers is an Executive Associate Dean of Academic Affairs and a Professor of Molecular and Cellular Biology at the College of Biological Sciences, UC Davis. His research focuses on mechanisms that regulate cell growth in the model eukaryote, the budding yeast S. cerevisiae, with particular emphasis on the TOR (target of rapamycin) signal transduction network. His work investigates how this network regulates the flow of genetic information and cellular behavior in response to intracellular and environmental cues. Dr. Powers holds a B.A. in Biochemistry and Molecular Biology from the University of California, Santa Cruz, obtained in 1985, and a Ph.D. in Biology from the same institution, earned in 1992. His contributions include building inroads with remote Pacific Islands that have led to the development of a powerful drug, and he is actively engaged in research related to cell growth regulation and signal transduction pathways.

Research topics

• Biology
• Cell biology
• Biochemistry
• Genetics
• Chemistry

Selected publications

• Conheça a história da rapamicina, medicamento de US$ 1 bi cuja ciência e a indústria farmacêutica devem aos indígenas da Ilha de Páscoa

  2025-09-30

  preprintOpen access1st authorCorresponding

  Câncer. Diabetes. O próprio envelhecimento. O potencial da rapamicina para tratar uma série de doenças tem sido uma fonte de fascínio científico. Mas muitos não conhecem suas origens e seu legado complicado

  PublisherDOI

• Comment un médicament essentiel de la médecine moderne a été découvert sur l'île de Pâques

  2025-10-02

  articleOpen access1st authorCorresponding
  PublisherDOI

• A billion-dollar drug was found in Easter Island soil – what scientists and companies owe the Indigenous people they studied

  2025-09-29

  preprintOpen access1st authorCorresponding
  PublisherDOI

• Metabolic Adaptations Determine the Evolutionary Trajectory of TOR Signaling in Diverse Eukaryotes

  Biomolecules · 2025-09-08

  articleOpen accessSenior authorCorresponding

  Eukaryotes use diverse nutrient acquisition strategies, including autotrophy, heterotrophy, mixotrophy, and symbiosis, which shape the evolution of cell regulatory networks. The Target of Rapamycin (TOR) kinase is a conserved growth regulator that in most species functions within two complexes, TORC1 and TORC2. TORC1 is broadly conserved and uniquely sensitive to rapamycin, whereas the evolutionary distribution of TORC2 is less well-defined. We built a sensitive hidden Markov model (HMM)-based pipeline to survey core TORC1 and TORC2 components across more than 800 sequenced eukaryotic genomes spanning multiple major supergroups. Both complexes are present in early-branching lineages, consistent with their presence in the last eukaryotic common ancestor, followed by multiple lineage-specific losses of TORC2 and, more rarely, TORC1. A striking pattern emerges in which TORC2 is uniformly absent from photosynthetic autotrophs derived from primary endosymbiosis and frequently lost in those derived from secondary or tertiary events. In contrast, TORC2 is consistently retained in mixotrophs, which obtain carbon from both photosynthesis and environmental uptake, and in free-living obligate heterotrophs. These findings suggest that TORC2 supports heterotrophic metabolism and is often dispensable under strict autotrophy. Our results provide a framework for the evolutionary divergence of TOR signaling and highlight metabolic and ecological pressures that shape TOR complex retention across eukaryotes.

  PublisherOA PDFDOI

• The origin story of rapamycin: systemic bias in biomedical research and cold war politics

  Molecular Biology of the Cell · 2022-10-13 · 22 citations

  articleOpen access1st authorCorresponding

  METEI (Medical Expedition to Easter Island) was a Canadian-led expedition to Easter Island in 1964 that led to the discovery of rapamycin, launching a billion-dollar drug industry and major field of biomedical research. Stanley’s Dream, by medical historian Jacalyn Duffin, provides remarkable details about METEI and raises important and timely questions about systemic bias in biomedical studies, the relationship between science and geopolitics, as well as obligations of pharmaceutical companies to indigenous communities. As such, this book is a must-read for those interested in the intersection of science and society as well as anyone who has used rapamycin, or one of many derivatives, in their laboratory or clinic.

  PublisherOA PDFDOI

• Comment on “Sterilizing immunity in the lung relies on targeting fungal apoptosis-like programmed cell death”

  Science · 2018-06-21 · 11 citations

  letter

  Shlezinger et al . (Reports, 8 September 2017, p. 1037) report that the common fungus Aspergillus fumigatus , a cause of aspergillosis, undergoes caspase-dependent apoptosis-like cell death triggered by lung neutrophils. However, the technologies they used do not provide reliable evidence that fungal cells die via a protease signaling cascade thwarted by a fungal caspase inhibitor homologous to human survivin.

  PublisherDOI

• Redesigning TOR Kinase to Explore the Structural Basis for TORC1 and TORC2 Assembly

  Biomolecules · 2018-06-01 · 12 citations

  articleOpen accessSenior authorCorresponding

  TOR is a serine/threonine protein kinase that assembles into distinct TOR Complexes 1 and 2 (TORC1 or TORC2) to regulate cell growth. In mammalian cells, a single mTOR incorporates stably into mTORC1 and mTORC2. By contrast, in Saccharomyces cerevisiae, two highly similar Tor1 and Tor2 proteins exist, where Tor1 assembles exclusively into TORC1 and Tor2 assembles preferentially into TORC2. To gain insight into TOR complex assembly, we used this bifurcation in yeast to identify structural elements within Tor1 and Tor2 that govern their complex specificity. We have identified a concise region of ~500 amino acids within the N-terminus of Tor2, which we term the Major Assembly Specificity (MAS) domain, that is sufficient to confer significant TORC2 activity when placed into an otherwise Tor1 protein. Consistently, introduction of the corresponding MAS domain from Tor1 into an otherwise Tor2 is sufficient to confer stable association with TORC1-specific components. Remarkably, much like mTOR, this latter chimera also retains stable interactions with TORC2 components, indicating that determinants throughout Tor1/Tor2 contribute to complex specificity. Our findings are in excellent agreement with recent ultrastructural studies of TORC1 and TORC2, where the MAS domain is involved in quaternary interactions important for complex formation and/or stability.

  PublisherOA PDFDOI

• Sterol transporters at membrane contact sites regulate TORC1 and TORC2 signaling

  The Journal of Cell Biology · 2017-08-03 · 107 citations

  articleOpen access

  Membrane contact sites (MCSs) function to facilitate the formation of membrane domains composed of specialized lipids, proteins, and nucleic acids. In cells, membrane domains regulate membrane dynamics and biochemical and signaling pathways. We and others identified a highly conserved family of sterol transport proteins (Ltc/Lam) localized at diverse MCSs. In this study, we describe data indicating that the yeast family members Ltc1 and Ltc3/4 function at the vacuole and plasma membrane, respectively, to create membrane domains that partition upstream regulators of the TORC1 and TORC2 signaling pathways to coordinate cellular stress responses with sterol homeostasis.

  PublisherOA PDFDOI

• Budding Yeast <i> <scp>S</scp> accharomyces Cerevisiae </i> as a Model Genetic Organism

  Encyclopedia of Life Sciences · 2017-11-07 · 5 citations

  other

  Abstract Budding yeast has served as an experimental organism for genetic research for over 50 years. The yeast shares a common cell division cycle and cellular architecture with other eukaryotes, and as a microorganism, it is easily propagated and manipulated in the laboratory. An intense focus on the central dogma, the cell cycle and sexual reproduction unleashed new fields including gene silencing, homologous recombination and differential gene expression, among others. The ease of genetic analysis allowed researchers to study processes to a degree not seen for other model organisms. As was often the case, new techniques were developed in yeast that are now broadly used. Budding yeast was the first eukaryote to be sequenced, which, in turn, led to genome‐wide analyses to map gene networks common to all life. Research on yeast has also informed us on the molecular basis of human diseases from birth defects to neurodegenerative disorders. Key Concepts Budding yeast is nonpathogenic, easy to grow and amenable to genetic analysis. Core cellular functions and cell architecture are highly conserved with other eukaryotes. Genes from other species can be expressed in yeast and function in place of the homologous yeast gene. Sexual reproduction allows for genetic recombination and recovery of haploid yeasts expressing recessive phenotypes. Homologous recombination is used to facilitate genome engineering. Many tools used in molecular biology were developed in yeast (e.g. yeast two‐hybrid assay). Budding yeast was the first eukaryote to have its entire genome sequenced. A vast amount of yeast information has been catalogued in the Saccharomyces Genome Database (SGD) and is readily accessible to anyone. The yeast knockout collection has been used for genome‐wide studies of gene function.

  PublisherDOI

• Mitochondrial respiration links TOR complex 2 signaling to calcium regulation and autophagy

  Autophagy · 2017-03-22 · 18 citations

  articleOpen accessSenior authorCorresponding

  The target of rapamycin (TOR) kinase is a conserved regulator of cell growth and functions within 2 different protein complexes, TORC1 and TORC2, where TORC2 positively controls macroautophagy/autophagy during amino acid starvation. Under these conditions, TORC2 signaling inhibits the activity of the calcium-regulated phosphatase calcineurin and promotes the general amino acid control (GAAC) response and autophagy. Here we demonstrate that TORC2 regulates calcineurin by controlling the respiratory activity of mitochondria. In particular, we find that mitochondrial oxidative stress affects the calcium channel regulatory protein Mid1, which we show is an essential upstream activator of calcineurin. Thus, these findings describe a novel regulation for autophagy that involves TORC2 signaling, mitochondrial respiration, and calcium homeostasis.

  PublisherOA PDFDOI

Recent grants

• TOR Complex 2 and sphingolipid biosynthesis.

  NIH · $1.3M · 2009–2015

• INNER CENTROMERE TARGETING OF THE CHROMOSOME PASSENGER COMPLEX

  NIH · $10.6M · 2011–2016

Frequent coauthors

• Harry F. Noller

  University of California, Santa Cruz

  13 shared

• Brad J. Niles

  University of California, Davis

  9 shared

• Sofia Aronova

  University of Minnesota

  8 shared

• Karen P. Wedaman

  University of California, Davis

  7 shared

• Ariadne Vlahakis

  University of California, San Francisco

  7 shared

• Michael N. Hall

  University of Basel

  6 shared

• Aaron W. Reinke

  University of Toronto

  5 shared

• Ivanka Dilova

  University of California, Davis

  5 shared

Awards & honors

• Annual Award and Citation Ceremony
• Storer Lectureship in the Life Sciences