Faculty Portrait

Contact Information

Name: Kimberly Mulligan

Title: Associate Professor

Office Location: TSC 4021

Email: kimberly.mulligan@csus.edu

Office Phone: (916) 278-4064

Mailing Address: Sacramento State 6000 J Street Sacramento, CA 95819-6077

Office Hours: Mon/Wed, 10:30am - 12:00pm (Spring 2023)

Where to find me : TSC 4021 (office), TSC 4027 (lab), or email me to meet via Zoom

Courses that I Teach

  • BIO 294A: Seminar in Molecular and Cellular Biology
  • BIO 220: Introduction to Scientific Inquiry
  • BIO 227: Development and Regenerative Medicine
  • BIO 127: Developmental Biology
  • BIO 121: Molecular Cell Biology
  • BIO 2 Lab: Cells, Molecules and Genes

Lab Homepage



U. Nguyen, B. Tinsley, Y. Sen, J. Stein, Y. Palacios, A. Ceballos, C. Welch, K. Nzenkue, A. Penn, L. Murphy, K. Leodones, J. Casiquin, I. Ivory, K. Ghenta, K. Danziger, E. Widman, J. Newman, M. Triplehorn, Z. Hindi, K. Mulligan (2021) Exposure to bisphenol A differentially impacts neurodevelopment and behavior in Drosophila melanogaster from distinct genetic backgrounds. NeuroToxicology, Volume 82, Pages 146-157,ISSN 0161-813X, https://doi.org/10.1016/j.neuro.2020.12.00

Poston RG, Murphy LN, Rejepova A, Ghaninejad-Esfahani M, Joshua Segales J, Mulligan K, Saha RN. (2020) Specific ortho-hydroxylated brominated ethers inhibit neuronal MEK-ERK signaling and disrupt neurodevelopmental processes J. Biol. Chem. 2020, jbc.RA119.011138. doi:10.1074/jbc.RA119.011138

Mulligan K and Cheyette B (2017) Neurodevelopmental Perspectives on Wnt Signaling in Psychiatry. Review. Mol Neuropsychiatry. Jan 13. (2) 219-246

Mulligan K and Cheyette B (2016) Introduction to Wnt signaling, Chapter for Inborn Errors of Development, 3rd Edition, Oxford University Press

Martin P, Stanley R, Ross A, Freitas A, Moyer C, Brumback A, Iafrati J, Stapornwongkul K, Dominguez S, Kivimae S, Mulligan K, Pirooznia M, McCombie W, Potash J, Zandi P, Purcell S, Sanders S, Zuo Y, Sohal V, Cheyette B (2016) DIXDC1 contributes to psychiatric susceptibility by regulating dendritic spine and glutamatergic synapse density via GSK3 and Wnt/β-catenin signaling Mol Psychiatry. Oct 18. doi: 10.1038

Mulligan K and Cheyette B (2012) Wnt signaling in vertebrate neural development and function Review. J NeuroImmune Pharmacol. Dec; 7(4) 774-87

Mulligan K, Fuerer C, Ching W, Willert K, Fish M, Nusse R (2012) Secreted-Wingless interacting molecule (Swim) promotes long-range signaling by maintaining Wingless solubility Proc Natl Acad Sci USA. Jan10;109(2):370-7

Nusse R, Fuerer C, Ching W, Harnish K*, Logan C, Zeng A, ten Berge D, Kalani Y. (2008) Wnt signaling and stem cell control Cold Spring Harb Symp Quant Biol. Nov (73) 59-66. Review

Johnson ML, Harnish K*, Nusse R, Van Hul W (2004) LRP5 and Wnt signaling: a union made for bone. J Bone Mineral Research. Nov;19(11):1749-57. Review

Research Projects/Interests

My lab is interested in understanding how genes and non-heritable environmental factors may converge to cause neurodevelopmental disorders, like autism spectrum disorders (ASD). ASD are a group of heterogeneous neurodevelopmental disorders defined by mild to severe impairments in communication, behavior, and social interactions. The prevalence of ASD has increased considerably over the past several decades, and the annual cost in the U.S. has more than tripled since 2006 to over $126 billion/year in 2012. Currently, 1 in every 68 children born in the U.S. are diagnosed with ASD.

ASD is a highly heritable complex disorder. Current estimates suggest dozens of genes contribute to the development of ASD. There is also mounting evidence that ASD is a multifactorial disorder that is often caused when multiple genes and environmental (epigenetic) factors converge to affect the normal neurodevelopmental program during prenatal brain development. The identification of epigenetic factors that confer risk to ASD and analysis of their molecular mechanisms could provide measures to prevent or decrease the severity of ASD. 

In our lab, we use the fruit fly Drosophila melanogaster to identify and examine candidate environmental chemicals to determine if they can impair neural development in flies that have genetic mutations associated with ASD. It is estimated that 75% of the genes associated with human disease are conserved in Drosophila, and they have already served as a model organism for the study of genes implicated in ASD in humans. Indeed, mutating  ASD susceptibility genes in flies can cause measurable social and behavioral deficits in the mutant flies. Fruit flies are also incredibly easy to manipulate genetically, making them ideal for the study of multiple genetic mutations in the same organism. There are a number of well-defined behavioral assays, one of the most prominent being the courtship assay. (Flies have specific, stereotyped behaviors they perform during courtship and alteration in these behaviors is often indicative of a change in neural circuitry.) If behavioral changes are detected in adult flies, brains and neurons can be examined to elucidate the mechanism by which a particular chemical alters brain development. Finally, fruit flies have a generation time from egg to adult of 9 days, so meaningful data can be generated relatively quickly; this is critical given the urgent need to understand the causes ASD. 

For more information, please visit my lab homepage.

Article About My Teaching Strategies



Whole larval brain

Full view of the fruit fly larval brain.

A lobe of the fruit fly larval brain with fluorescently marked neural stem cells.

 A lobe of the fruit fly larval brain with fluorescently marked neural stem cells.