Donald E. Ayer

Donald E. Ayer, PhD

Languages spoken: English

Academic Information

Departments Primary - Oncological Sciences

Lab

Donald Ayer, PhD, is an investigator at Huntsman Cancer Institute (HCI) and a professor in the Department of Oncological Sciences at the University of Utah (U of U). He is a member of the Nuclear Control of Cell Growth and Differentiation Program.

Ayer is a leader in the area of gene regulation and its role in normal and cancer cell growth. His research focuses on how cells regulate a transcription factor known as Myc, which is mutated in a wide variety of cancers. In normal cells, Myc is responsible for turning on the genes that are required for cell division. In cancer cells, Myc is "hyperactive" and causes cells to divide continuously, creating excess, unnecessary cells that form a tumor. Ayer's research group investigates how Myc functions in normal and cancer cells, and they work to increase the understanding of basic gene control mechanisms. This information could greatly improve cancer diagnosis methods and treatment.

Ayer, a native of Michigan, earned a PhD in chemistry and biochemistry from the University of Colorado. From 1989 to 1995, he received additional training under the direction of Robert Eisenman, PhD, a National Academy of Science member, at the Fred Hutchinson Cancer Research Center in Seattle. In 1995, he was recruited to the U of U and HCI.

Education History

Undergraduate University of Michigan
 BS
Doctoral Training University of Colorado
 PhD
Postdoctoral Fellowship Fred Hutchinson Cancer Research Center
 Postdoctoral Fellow

Selected Publications

Journal Article

  1. Han KS, Ayer DE (2013). MondoA senses adenine nucleotides: transcriptional induction of thioredoxin-interacting protein. Biochem J, 453(2), 209-18.
  2. Wilde BR, Ayer DE (2015). Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis. Br J Cancer, 113(11), 1529-33.
  3. Silveira AC, Hurst DR, Vaidya KS, Ayer DE, Welch D (2009). Over-expression of the BRMS1 family member SUDS3 does not suppress metastasis of human cancer cells. Cancer letters, 276(1), 32-7.
  4. Ayer DE, Kretzner L, Eisenman R (1993). Mad: a heterodimeric partner for Max that antagonizes Myc transcriptional activity. Cell, 72(2), 211-22.
  5. Hassig CA, Fleischer TC, Billin AN, Schreiber SL, Ayer D (1997). Histone deacetylase activity is required for full transcriptional repression by mSin3A. Cell, 89(3), 341-7.
  6. Ayer DE, Lawrence QA, Eisenman R (1995). Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3. Cell, 80(5), 767-776.
  7. Sullivan WJ, Mullen PJ, Schmid EW, Flores A, Momcilovic M, Sharpley MS, Jelinek D, Whiteley AE, Maxwell MB, Wilde BR, Banerjee U, Coller HA, Shackelford DB, Braas D, Ayer DE, de Aguiar Vallim TQ, Lowry WE, Christofk H (2018). Extracellular Matrix Remodeling Regulates Glucose Metabolism through TXNIP Destabilization. Cell, 175(1), 117-132.e21.
  8. Ayer DE, Eisenman R (1993). A switch from Myc:Max to Mad:Max heterocomplexes accompanies monocyte/macrophage differentiation. Genes & development, 7(11), 2110-9.
  9. Stoltzman CA, Kaadige MR, Peterson CW, Ayer D (2011). MondoA senses non-glucose sugars: regulation of thioredoxin-interacting protein (TXNIP) and the hexose transport curb. The Journal of biological chemistry, 286(44), 38027-34.
  10. Peterson CW, Stoltzman CA, Sighinolfi MP, Han KS, Ayer D (2010). Glucose controls nuclear accumulation, promoter binding, and transcriptional activity of the MondoA-Mlx heterodimer. Molecular and cellular biology, 30(12), 2887-95.
  11. Kaadige MR, Yang J, Wilde BR, Ayer D (2015). MondoA-Mlx transcriptional activity is limited by mTOR-MondoA interaction. Molecular and cellular biology, 35(1), 101-10.
  12. Ye Z, Ayer D (2018). Ras Suppresses TXNIP Expression by Restricting Ribosome Translocation. Molecular and cellular biology, 38(20),
  13. Stoltzman CA, Peterson CW, Breen KT, Muoio DM, Billin AN, Ayer D (2008). Glucose sensing by MondoA:Mlx complexes: a role for hexokinases and direct regulation of thioredoxin-interacting protein expression. Proceedings of the National Academy of Sciences of the United States of America, 105(19), 6912-7.
  14. Kaadige MR, Looper RE, Kamalanaadhan S, Ayer D (2009). Glutamine-dependent anapleurosis dictates glucose uptake and cell growth by regulating MondoA transcriptional activity. Proceedings of the National Academy of Sciences of the United States of America, 106(35), 14878-83.
  15. Shen L, O'Shea JM, Kaadige MR, Cunha S, Wilde BR, Cohen AL, Welm AL, Ayer D (2015). Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP. Proceedings of the National Academy of Sciences of the United States of America, 112(17), 5425-30.
  16. Bowman CJ, Ayer DE, Dynlacht B (2014). Foxk proteins repress the initiation of starvation-induced atrophy and autophagy programs. Nature cell biology, 16(12), 1202-14.
  17. Carroll PA, Diolaiti D, McFerrin L, Gu H, Djukovic D, Du J, Cheng PF, Anderson S, Ulrich M, Hurley JB, Raftery D, Ayer DE, Eisenman R (2015). Deregulated Myc requires MondoA/Mlx for metabolic reprogramming and tumorigenesis. Cancer cell, 27(2), 271-85.
  18. Chen JL, Merl D, Peterson CW, Wu J, Liu PY, Yin H, Muoio DM, Ayer DE, West M, Chi J (2010). Lactic acidosis triggers starvation response with paradoxical induction of TXNIP through MondoA. PLoS genetics, 6(9), e1001093.
  19. Sloan EJ, Ayer D (2010). Myc, mondo, and metabolism. Genes & cancer, 1(6), 587-96.
  20. Elgort MG, O'Shea JM, Jiang Y, Ayer D (2010). Transcriptional and Translational Downregulation of Thioredoxin Interacting Protein Is Required for Metabolic Reprogramming during G(1). Genes & cancer, 1(9), 893-907.
  21. Kaadige MR, Elgort MG, Ayer D (2010). Coordination of glucose and glutamine utilization by an expanded Myc network. Transcription, 1(1), 36-40.
  22. Parmenter TJ, Kleinschmidt M, Kinross KM, Bond ST, Li J, Kaadige MR, Rao A, Sheppard KE, Hugo W, Pupo GM, Pearson RB, McGee SL, Long GV, Scolyer RA, Rizos H, Lo RS, Cullinane C, Ayer DE, Ribas A, Johnstone RW, Hicks RJ, McArthur G (2014). Response of BRAF-mutant melanoma to BRAF inhibition is mediated by a network of transcriptional regulators of glycolysis. Cancer discovery, 4(4), 423-33.
  23. O'Shea JM, Ayer D (2013). Coordination of nutrient availability and utilization by MAX- and MLX-centered transcription networks. Cold Spring Harbor perspectives in medicine, 3(9), a014258.
  24. Wilde BR, Ye Z, Lim TY, Ayer D (2019). Cellular acidosis triggers human MondoA transcriptional activity by driving mitochondrial ATP production. eLife, 8,
  25. Peterson CW, Ayer D (2011). An extended Myc network contributes to glucose homeostasis in cancer and diabetes. Frontiers in bioscience (Landmark edition), 16, 2206-23.
  26. Schaub FX, Dhankani V, Berger AC, Trivedi M, Richardson AB, Shaw R, Zhao W, Zhang X, Ventura A, Liu Y, Ayer DE, Hurlin PJ, Cherniack AD, Eisenman RN, Bernard B, Grandori C, Cancer Genome Atlas Network (2018). Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas. Cell systems, 6(3), 282-300.e2.
  27. Ahn B, Wan S, Jaiswal N, Vega RB, Ayer DE, Titchenell PM, Han X, Won KJ, Kelly D (2019). MondoA drives muscle lipid accumulation and insulin resistance. JCI insight, 5,
  28. Lim TY, Wilde BR, Thomas ML, Murphy KE, Vahrenkamp JM, Conway ME, Varley KE, Gertz J, Ayer D (2023). TXNIP loss expands Myc-dependent transcriptional programs by increasing Myc genomic binding. PLoS biology, 21(3), e3001778.
  29. Van Scoyk AN, Antelope O, Ayer DE, Peterson RT, Pomicter AD, Owen SC, Deininger M (2024). Bioluminescence assay of lysine deacylase sirtuin activity. Cell chemical biology, 31(11), 2002-2014.e4.
  30. Yamamoto-Imoto H, Minami S, Shioda T, Yamashita Y, Sakai S, Maeda S, Yamamoto T, Oki S, Takashima M, Yamamuro T, Yanagawa K, Edahiro R, Iwatani M, So M, Tokumura A, Abe T, Imamura R, Nonomura N, Okada Y, Ayer DE, Ogawa H, Hara E, Takabatake Y, Isaka Y, Nakamura S, Yoshimori (2022). Age-associated decline of MondoA drives cellular senescence through impaired autophagy and mitochondrial homeostasis. Cell reports, 38(9), 110444.
  31. Wilde BR, Kaadige MR, Guillen KP, Butterfield A, Welm BE, Ayer D (2020). Protein synthesis inhibitors stimulate MondoA transcriptional activity by driving an accumulation of glucose 6-phosphate. Cancer & metabolism, 8(1), 27.
  32. Carroll PA, Freie BW, Cheng PF, Kasinathan S, Gu H, Hedrich T, Dowdle JA, Venkataramani V, Ramani V, Wu X, Raftery D, Shendure J, Ayer DE, Muller CH, Eisenman R (2021). The glucose-sensing transcription factor MLX balances metabolism and stress to suppress apoptosis and maintain spermatogenesis. PLoS biology, 19(10), e3001085.
  33. Ayer DE, Lawrence QA, Eisenman R (1995). Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3. Cell, 80(5), 767-76.

Review

  1. McArthur GA, Laherty CD, Quéva C, Hurlin PJ, Loo L, James L, Grandori C, Gallant P, Shiio Y, Hokanson WC, Bush AC, Cheng PF, Lawrence QA, Pulverer B, Koskinen PJ, Foley KP, Ayer DE, Eisenman R (1998). The Mad protein family links transcriptional repression to cell differentiation. Cold Spring Harbor symposia on quantitative biology, 63, 423-33.

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