Biology subjects

Chitturi, J.

Publications and source records attributed to Chitturi, J..

5 recordsLinked to original sources

bioRxiv2026

Short-term forecasts of Aedes aegypti relative abundance to enhance mosquito control situational awareness

Conventional mosquito surveillance typically relies on contemporaneous data, making it challenging to anticipate future vector surges. To support proactive vector management, this study evaluates a multi-model forecasting framework designed to generate probabilistic 1-to 4-week-ahead forecasts of Aedes aegypti relative abundance per trap night. The framework was validated using multi-year surveillance data across four US jurisdictions spanning varied environments (from subtropical to temperate and arid). We found that an ensemble approach aggregating statistical and machine learning models generally achieved the best performance across all locations and forecast horizons. Relative forecast performance improved as the forecast horizon extended from 1 to 4 weeks ahead. The most challenging data to forecast were primarily restricted to low mosquito activity periods or atypical population peaks with unusual timing or magnitude. While full integration into routine vector management workflows represents a long-term process requiring operational adaptation, this work advances forecasting research and establishes a baseline for translating these approaches into real-time applications for public health authorities, with downstream effects in mitigating the risks of mosquito-borne diseases.

ecology↗

bioRxiv2025

Evaluating Field Trial Designs for Genetically Modified Mosquito Interventions: An In-Silico Simulation Approach

Mosquito control strategies based on the mass release of modified males, such as genetically modified mosquitoes (GMMs), aim to suppress wild populations by impairing reproduction. Evaluating these interventions requires resource-intensive field trials, but a lack of standardized implementation practices, particularly regarding release ratios of modified males to wild female mosquitoes and trial timing, has led to variable outcomes. This studys objective is to propose a modeling tool for the "in-silico" simulation of trial designs before field implementation. To this aim, we developed an agent-based model of mosquito population dynamics. As a case study, we calibrated the model using 2019-2023 Aedes aegypti surveillance data from Miami-Dade County, Florida, and compared two GMM trial designs as illustrative examples. Our results show that depending on the implementation choices (e.g., trial start date and duration, release ratio), trials yield highly variable outcomes. For example, changing the start date while fixing all other implementation details can lead to effectiveness between 50% and 90%. Our findings suggest that "in-silico" simulation is a valuable tool for improving trial protocol design, allowing stakeholders to test strategies and reduce outcome uncertainty before committing to a fieldwork experiment.

ecology↗

bioRxiv2023

The ubiquitin ligase UBR-1 regulates the synaptic strength between the GABAergic and glutamatergic signaling

Excitation/Inhibition (E/I) balance is carefully maintained by the nervous system. Neurotransmitter GABA has been reported to be co-released with its sole precursor, another neurotransmitter glutamate. The genetic and circuitry mechanisms to establish the balance between GABAergic and Glutamatergic signaling have not fully elucidated. C. elegans DVB is a classically defined excitatory GABAergic motoneuron that drives the expulsion step in defecation motor program. We show that in addition to UNC-47, the vesicular GABA transporter, DVB also expresses EAT-4, a vesicular glutamate transporter. UBR-1, a conserved ubiquitin ligase, regulates the DVB activity by suppressing a bidirectional inhibitory glutamate signaling. Loss of UBR-1 impairs the DVB Ca2+ activity and the expulsion frequency. These impairments are fully compensated by the knock-down of EAT-4 in DVB. Further, glutamate-gated chloride channels GLC-3 and GLC-2/4 receive DVBs glutamate signals to inhibit DVB and enteric muscle, respectively. These results implicate an intrinsic cellular mechanism that promotes the inherent asymmetric neural activity. We propose that the elevated glutamate in ubr-1 being the cause of the E/I shift, potentially contributes to the Johanson Blizzard Syndrome.

neuroscience↗

bioRxiv2022

K2P channel TWK-40 Regulates a Rhythmic Behavior in C. elegans

Leak potassium (K+) currents, conducted by two-pore domain K+ (K2P) channels, are critical for the stabilization of the membrane potential. The effect of K2P channels on motor rhythm remains enigmatic. We show here that the K2P TWK-40 regulates the rhythmic defecation motor program (DMP) in Caenorhabditis elegans. Disrupting TWK-40 suppresses the expulsion defects of nlp-40 and aex-2 mutants. By contrast, a gain-of-function (gf) mutant of twk-40 significantly reduces the expulsion frequency per DMP cycle. In situ whole-cell patch clamping demonstrates that TWK-40 forms an outward current that hyperpolarize the resting membrane potential of DVB neuron. In addition, TWK-40 substantially contributes to the rhythmic activity of DVB. Specifically, DVB Ca2+ oscillations exhibit obvious defects in twk-40 mutants. Expression of TWK-40(gf) in DVB recapitulates the expulsion deficiency of the twk-40(gf) mutant, and inhibits DVB Ca2+ oscillations in both wild-type and twk-40(lf) animals. Moreover, DVB innervated enteric muscles also exhibit rhythmic Ca2+ defects. Taken together, these results demonstrate that TWK-40 is an essential neuronal inhibitor of DMP, thus revealing a cellular mechanism linking leak K2P channels with rhythmic motor activity.

neuroscience↗

bioRxiv2018

The UBR-1 Ubiquitin Ligase Regulates Glutamate Metabolism to Generate Coordinated Motor Pattern in C. elegans

UBR1 is an E3 ubiquitin ligase best known for its ability to target protein degradation by the N-end rule. The physiological functions of UBR family proteins, however, remain not fully understood. We found that the functional loss of C. elegans UBR-1 leads to a specific motor deficit: when adult animals generate reversal movements, A-class motor neurons exhibit synchronized activation, preventing body bending. This motor deficit is rescued by removing GOT-1, a transaminase that converts aspartate to glutamate. Both UBR-1 and GOT-1 are expressed and critically required in premotor interneurons of the reversal motor circuit to regulate the motor pattern. ubr-1 and got-1 mutants exhibit elevated and decreased glutamate level, respectively. These results raise an intriguing possibility that UBR proteins regulate glutamate metabolism, which is critical for neuronal development and signaling.\n\nAuthor SummaryUbiquitin-mediated protein degradation is central to diverse biological processes. The selection of substrates for degradation is carried out by the E3 ubiquitin ligases, which target specific groups of proteins for ubiquitination. The human genome encodes hundreds of E3 ligases; many exhibit sequence conservation across animal species, including one such ligase called UBR1. Patients carrying mutations in UBR1 exhibit severe systemic defects, but the biology behinds UBR1s physiological function remains elusive. Here we found that the C. elegans UBR-1 regulates glutamate level. When UBR-1 is defective, C. elegans exhibits increased glutamate; this leads to synchronization of motor neuron activity, hence defective locomotion when animals reach adulthood. UBR1-mediated glutamate metabolism may contribute to the physiological defects of UBR1 mutations.

neuroscience↗