About

Joanna C. Chiu, Ph.D., is a Professor and Chair of the Department of Entomology and Nematology at the College of Agricultural and Environmental Sciences, UC Davis. She is also the Principal Investigator of her own lab and affiliated with the UC Davis Genome Center and the UC San Diego Center for Circadian Biology. Dr. Chiu received her Bachelor of Arts degree from Mount Holyoke College with double majors in Biology and Music. She earned her Ph.D. in molecular genetics from the Department of Biology at New York University, where her thesis research focused on understanding the function of glutamate receptor genes in plants using Arabidopsis thaliana as a model organism. Although she initially pursued plant research, her passion shifted towards studying how genes and proteins regulate animal behavior, particularly in the field of circadian biology. Circadian rhythms, which are endogenously driven and present in organisms ranging from bacteria to mammals, regulate daily physiological states and activities such as sleep and feeding. To investigate the molecular mechanisms underlying circadian rhythms, Dr. Chiu conducted postdoctoral research at Rutgers University, studying how posttranslational mechanisms of clock proteins regulate these rhythms. Currently, her lab at UC Davis continues to explore the regulation of animal circadian and seasonal rhythms using a combination of molecular genetics, biochemical, and proteomic approaches. Her research aims to elucidate the molecular pathways and mechanisms that control circadian timing and seasonal adaptations in animals.

Research topics

• Biology
• Evolutionary biology
• Genetics
• Ecology
• Botany
• Physiology
• Horticulture
• Agronomy
• Neuroscience
• Agroforestry

Selected publications

• Biological timing: Changing photoperiods select for self-sustaining clocks

  Current Biology · 2026-03-01

  articleSenior author
  PublisherDOI

• Divergent signaling profiles in mTOR gain-of-function Smith-Kingsmore syndrome (SKS) and TSC2 deficiency

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-13

  articleOpen access

  Abstract Smith-Kingsmore syndrome (SKS) is a rare neurodevelopmental disorder caused by gain-of-function mutations in MTOR , yet whether these mutations phenocopy TSC2 loss or establish a distinct signaling state remains unclear. Using quantitative proteomics, phosphoproteomics, and transcriptomics in isogenic cell models of SKS ( MTOR Δ4aa ), TSC2 loss ( TSC2 −/– ), and wild-type controls under glucose depletion and refeeding, we find that MTOR Δ4aa and TSC2 −/– cells occupy fundamentally distinct regulatory states. TSC2 −/– cells exhibit broad anabolic remodeling and a transcriptional program dominated by NF-κB- and STAT-driven inflammatory responses. MTOR Δ4aa cells instead display enrichment of nuclear and RNA processing programs, E2F/MYC-driven transcription, and a constrained proteomic dynamic range across nutrient states. Phosphoproteomic analysis of MTOR Δ4aa reveals rerouting of nutrient-responsive signaling toward MAPK/ERK- and Ca 2+ /CaMK-dependent pathways with limited canonical mTORC1/S6K1 engagement. These findings establish SKS as a signaling rewiring disorder distinct from classical mTORC1 hyperactivation, with implications for therapeutic targeting.

  PublisherOA PDFDOI

• Circadian clock gates diurnal glucose utilization

  PLoS Biology · 2026-04-17

  articleOpen accessSenior author

  The circadian clock and cellular metabolism are tightly coupled to maintain homeostasis. A new study in PLOS Biology leverages metabolic tracing to reveal time-of-day-dependent activities of glucose metabolic pathways in Drosophila that are disrupted in clock and sleep mutants.

  PublisherDOI

• P130 SAFETY AND EFFICACY OF DIRECT ORAL ANTICOAGULANTS VERSUS VITAMIN K ANTAGONISTS IN PATIENTS WITH FRAILTY AND ATRIAL FIBRILLATION: A SYSTEMATIC REVIEW AND META-ANALYSIS

  Canadian Journal of Cardiology · 2025-10-01

  article
  PublisherDOI

• Population genomics of Aedes albopictus across remote Pacific islands for genetic biocontrol considerations

  PLoS neglected tropical diseases · 2025-08-11 · 5 citations

  articleOpen accessCorresponding

  Remote Pacific islands (RPI) are characterized by ecological isolation, diverse endemic species, and vulnerability to invasive organisms due to globalization-driven connectivity. Among these species, Aedes albopictus, a highly invasive vector of flaviviruses, has spread extensively across the RPI via human-mediated dispersal, posing significant health and economic burdens. While the population structure and the degree of gene flow between mosquito populations can inform the dispersal pathways critical for disease vector management, the population genetics of Ae. albopictus in Northern RPI remains understudied. The present work investigated the population structure and connectivity of Ae. albopictus populations from Guam, Hawaiian Islands, and the Republic of the Marshall Islands (RMI) to inform disease and vector-based biosecurity risks and develop targeted management strategies. This is the first assessment to develop and analyze whole genome sequences of Ae. albopictus for RPI, enabling more accurate estimates of differentiation, admixture, and ancestry. We found distinct genetic clustering between regions, distinct ancestry of populations across RPI, and potential invasions that originated from Hawaii and spread into the RMI, and invasions from North America that spread to Guam. These findings can inform biosecurity protocols to limit the invasion of Ae. albopictus and their associated diseases within Hawaii and around the Pacific. Given the significant degree of genetic differentiation, we found between islets, islands, and regions, the genome data from this study can be used to enable the development of locally confined geographically isolated gene drives. These drives may be used to prevent and control outbreaks of dengue, chikungunya, and Zika, diseases that have had devastating consequences in these remote island communities.

  PublisherDOI

• Global changes in alternative splicing are associated with insecticide response and resistance

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-23

  preprintOpen accessSenior authorCorresponding

  Abstract Alternative splicing (AS) promotes phenotypic plasticity to adverse conditions by altering transcripts involved in stress adaptation. However, whether changes in AS occur transcriptome-wide or in only a few key genes is unclear. Agricultural insect pests are regularly exposed to xenobiotic stress from insecticide applications and thus develop resistance. We show that the pest Drosophila suzukii, resistant to multiple insecticides, exhibits increased global AS events compared to susceptible flies. Alternatively spliced genes are enriched in multiple processes including stress response and insecticide resistance, suggesting AS is a mechanism underlying insecticide resistance development. Furthermore, sublethal insecticide exposure promotes AS events even in the absence of substantial differential gene expression. This study provides insights into the role of AS in enabling insects to diversify genome function to survive acute insecticide treatment and to develop xenobiotic resistance.

  PublisherDOI

• Splicing of a core clock gene regulates seasonal adaptations by a winter gating mechanism

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-11-08

  preprintOpen accessSenior authorCorresponding

  Abstract Seasons bring changes to the environment. Many organisms adjust their physiology and behavior in response to seasonal changes in order to survive. Although the molecular mechanisms mediating the integration of seasonal cues are still unclear, the working model indicates the involvement of the circadian clock. Notably, the circadian neuropeptide Pigment Dispersing Factor (PDF), an output of the circadian clock, has been shown to alter its expression and activity in response to seasonal changes to facilitate seasonal adaptations in insects. Here, we show that the alternative splicing (AS) of a circadian clock gene, timeless (tim) , regulates the seasonal responses of PDF signaling in Drosophila melanogaster . We first showed that tim-sc, the predominant isoform in winter, is regulated by photoperiod in addition to temperature, while the expression of the canonical tim-l isoform is primarily sensitive to temperature. We then demonstrated that tim-sc maintains physiology and behavior in a “winter lock” state by modulating PDF. At the cellular and molecular level, TIM-SC behavior differs from the canonical TIM-L. Interestingly, flies expressing tim-sc did not fully phenocopy wild-type flies reared in winter conditions, suggesting that other mechanisms are at play in regulating seasonal adaptations, despite the importance of tim AS.

  PublisherDOI

• The soluble epoxide hydrolase inhibitor TPPU alleviates Aβ-mediated neuroinflammatory responses in Drosophila melanogaster and cellular models of alzheimer’s disease

  Journal of Inflammation · 2025-06-23 · 2 citations

  articleOpen access

  BACKGROUND: Alzheimer's disease (AD) is a common neurodegenerative disease, and its pathogenesis is closely associated with neuroinflammation. The control of neuroinflammation in AD is the focus of current research. soluble epoxide hydrolase (sEH) protein is increased in the brain tissues of patients with AD and has been targeted by multiple genome wide association studies as a prime target for treating AD. Since sEH induces nerve inflammation by degrading epoxyeicosatrienoic acids (EETs), application of sEH inhibitor and sEH gene knockout are effective ways to improve the bioavailability of EETs and inhibit or even resolve neuroinflammation in AD. 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU) is a potent sEH inhibitor that has been shown to be effective in preclinical animal models of a variety of chronic inflammatory diseases. This study aims to further explore whether TPPU can alleviate AD neuroinflammation. METHODS: We established an Aβ42-transgenic Drosophila melanogaster model using the galactose-regulated upstream promoter element 4 (GAL4) / upstream active sequence (UAS) expression system and investigated the protective and anti-neuroinflammatory effects of TPPU against Aβ toxicity. We detected behavioral indexes (survival time, crawling ability, and olfactory memory) and biochemical indexes malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in brain tissues of Aβ42 transgenic flies. Finally, we explored the anti-neuroinflammatory effect of TPPU and its possible mechanism by stimulating cocultures of human SH-SY5Y cells and HMC3 cells with Aβ(25-35) to model neuronal cell inflammation, and evaluated the cells by fluorescence microscopy, ELISA, Western Blot, and Real-time PCR. RESULTS: We found that TPPU improved the survival time, crawling ability, and olfactory memory of Aβ42-transgenic flies. We also observed reduction of MDA content and elevation of SOD activity in the brain tissues of these flies. In human cell models, we found that TPPU improved cell viability, reduced cell apoptosis, decreased lipid oxidation, inhibited oxidative damage, thus playing a neuroprotective role. The inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and interleukin-18 (IL-18) were downregulated, and the mRNA expression of the M2 microglia markers CD206 and SOCS3 were upregulated by TPPU; thus, TPPU inhibited neuroinflammatory responses. TPPU exerted neuroprotective and anti-inflammatory effects by decreasing the protein expression of the sEH-encoding gene EPHX2 and increasing the levels of 11,12-epoxyeicosatrienoic acid (11,12-EET) and 14,15-epoxyeicosatrienoic acid (14,15-EET). The inhibitory effect of TPPU on Aβ(25-35)-mediated neuroinflammation was associated with inhibition of the toll like receptor 4 (TLR4)/nuclear transcription factor-κB (NF-κB) pathway and p38 mitogen activated protein kinases (MAPK)/NF-κB pathway. CONCLUSIONS: We report that the sEH inhibitor TPPU exerts neuroprotective and anti-neuroinflammatory effects in AD models, and it is expected that this drug could potentially be used for the prevention and treatment of AD.

  PublisherOA PDFDOI

• O-GlcNAcylation of nuclear proteins in the mouse liver exhibit daily oscillations that are influenced by meal timing

  PLoS Biology · 2025-09-25 · 4 citations

  articleOpen accessSenior authorCorresponding

  The liver circadian clock and hepatic transcriptome are highly responsive to metabolic signals generated from feeding-fasting rhythm. Previous studies have identified a number of nutrient-sensitive signaling pathways that could interpret metabolic input to regulate rhythmic hepatic biology. Here, we investigated the role of O-GlcNAcylation, a nutrient-sensitive post-translational modification (PTM) in mediating metabolic regulation of rhythmic biology in the liver. We observe daily oscillation of global nuclear protein O-GlcNAcylation in the liver of mice subjected to night-restricted feeding (NRF) using label-free global O-GlcNAc proteomics. Additional site-specific O-GlcNAc analysis by tandem mass tag mass spectrometry further supports temporal differences in O-GlcNAcylation by revealing day-night differences. Proteins involved in gene expression are enriched among rhythmically O-GlcNAcylated proteins, suggesting rhythmic O-GlcNAcylation may directly regulate the hepatic transcriptome. We show that rhythmic O-GlcNAcylation can also indirectly modulate nuclear proteins by interacting with phosphorylation. Several proteins harboring O-GlcNAcylation-phosphorylation interplay motif exhibit rhythmic O-GlcNAcylation and phosphorylation. Specifically, we show that O-GlcNAcylation occurs at a phospho-degron of a key circadian transcriptional activator, circadian locomotor output cycles kaput (CLOCK), thus regulating its stability and transcriptional output. Finally, we report that day-restricted feeding (DRF) in the nocturnal mouse significantly alters O-GlcNAcylation pattern. Whereas global O-GlcNAcylation analysis indicates dampening of global O-GlcNAcylation rhythm in mice fed under DRF, site-specific analysis reveals differential responses of O-GlcNAc sites when timing of food intake is altered. Notably, a substantial number of O-GlcNAcylation sites exhibit inverted day-night profiles when mice are subjected to DRF. This suggests the dysregulation of daily nuclear protein O-GlcNAcylation rhythm may contribute to the disruption in liver transcriptome previously observed in DRF condition. In summary, our results provide new mechanistic insights into metabolic regulation of hepatic transcriptional regulators via interplay between O-GlcNAcylation and phosphorylation and shed light on the deleterious effects of improper mealtimes.

  PublisherDOI

• Reviewer #1 (Public Review): Taste triggers a homeostatic temperature control in Drosophila

  2024-02-28

  peer-reviewOpen access

  Hungry animals consistently show a desperate desire to obtain food. Even a brief sensory detection of food can trigger bursts of physiological and behavioral changes. However, the underlying mechanisms by which the sensation of food triggers the acute behavioral response remain elusive. We have previously shown in Drosophila that hunger drives a preference for low temperature. Because Drosophila is a small ectotherm, a preference for low temperature implies a low body temperature and a low metabolic rate. Here, we show that taste sensing triggers a switch from a low to a high temperature preference in hungry flies. We show that taste stimulation by artificial sweeteners or optogenetics triggers an acute warm preference, but is not sufficient to reach the fed state. Instead, nutrient intake is required to reach the fed state. The data suggest that starvation recovery is controlled by two components: taste-evoked and nutrient-induced warm preferences, and that taste and nutrient quality play distinct roles in starvation recovery. Animals are motivated to eat based on time of day or hunger. We found that clock genes and hunger signals profoundly control the taste-evoked warm preferences. Thus, our data suggest that the taste-evoked response is one of the critical layers of regulatory mechanisms representing internal energy homeostasis and metabolism.

  PublisherOA PDFDOI

Recent grants

• NIH Grant K99NS061952

  NIH · $176k · 2010

• A comparative proteomic approach to understand animal circadian clock

  NSF · $772k · 2015–2020

• Non-transcriptional regulation of circadian physiology

  NIH · $3.1M · 2019–2028

• NIH Grant F32NS049862

  NIH · $93k · 2007

• The role of DBT and NEMO-dependent phosphoproteome in regulating animal clockwork

  NIH · $1.4M · 2013–2019

Frequent coauthors

• Sergio Hidalgo

  University of California, Davis

  32 shared

• Erika Nguyen

  University of California, Davis

  21 shared

• Sheena S. Uchino

  21 shared

• Jay Suh

  University of Bonn

  21 shared

• Yujiro Umezaki

  University of Bonn

  21 shared

• Isaac Edery

  Rutgers, The State University of New Jersey

  20 shared

• Christine A. Tabuloc

  University of California, Davis

  20 shared

• Yoosook Lee

  Florida Medical Entomology Laboratory

  18 shared

Labs

• Joanna C. Chiu LabPI

Education

• PhD, Biology - Molecular Genetics

  New York University

  2004

• BA magna cum laude, Biology and Music

  Mount Holyoke College

  1995