Biology subjects

Chiu, G.

Publications and source records attributed to Chiu, G..

4 recordsLinked to original sources

bioRxiv2024

Unifying community-wide whole-brain imaging datasets enables robust automated neuron identification and reveals determinants of neuron positioning in C. elegans

We develop a data harmonization approach for C. elegans volumetric microscopy data, still or video, consisting of a standardized format, data pre-processing techniques, and a set of human-in-the-loop machine learning based analysis software tools. We unify a diverse collection of 118 whole-brain neural activity imaging datasets from 5 labs, storing these and accompanying tools in an online repository called WormID (wormid.org). We use this repository to train three existing automated cell identification algorithms to, for the first time, enable accuracy in neural identification that generalizes across labs, approaching human performance in some cases. We mine this repository to identify factors that influence the developmental positioning of neurons. To facilitate communal use of this repository, we created open-source software, code, web-based tools, and tutorials to explore and curate datasets for contribution to the scientific community. This repository provides a growing resource for experimentalists, theorists, and toolmakers to (a) study neuroanatomical organization and neural activity across diverse experimental paradigms, (b) develop and benchmark algorithms for automated neuron detection, segmentation, cell identification, tracking, and activity extraction, and (c) inform models of neurobiological development and function.

neuroscience↗

bioRxiv2023

Ontogenetic Patterns in Juvenile Blue Crab density: Effects of Habitat and Turbidity in a Chesapeake Bay Tributary

Nursery habitats are characterized by favorable conditions for juveniles, such as higher food availability and lower predation risk, and dispropor-tionately contribute more individuals per unit area to adult segments of the population compared to other habitats. However, nursery habitat inference is complicated by changes in habitat preferences with ontogeny; individuals in early-life stages frequently inhabit different habitats than older juveniles or adults. In this mensurative field experiment, we modeled the density of two juvenile blue crab, Callinectes sapidus, size classes based on carapace width (CW) across multiple habitats at various locations within an estuarine seascape during the blue crab recruitment season. We examined four habi-tat types--unstructured sand, seagrass meadows, salt marsh edge (SME), and shallow detrital habitat (SDH). Results indicated that densities of small ju-venile blue crabs ([≤]15 mm CW) were highest in seagrass, whereas densities of larger juveniles (16-30 mm CW) were highest in SME. Densities of large juveniles in SME were also greater than those of small juveniles, suggest-ing possible secondary dispersal to SME by small juveniles after settlement and recruitment in seagrass. Turbidity was positively correlated with densi-ties of both size classes, although our model did not address whether this was due to top-down (refuge) or bottom-up (food availability) mechanisms. Ob-served patterns in size-specific habitat utilization may result from changing requirements of juvenile blue crabs with size, as animals minimize mortality-to-growth ratios. Taken together with previous work and patterns observed in SME, these findings emphasize the role of salt marsh habitat within juve-nile blue crab ontogeny and underscore the need to quantify and preserve the complete chain of habitats used by juveniles.

ecology↗

bioRxiv2021

Concerted cellular responses to type I interferon propel memory impairment associated with amyloid β plaques

Despite well-documented maladaptive neuroinflammation in Alzheimers disease (AD), the principal signal that drives memory and cognitive impairment remains elusive. Here, we reveal robust, age-dependent cellular reactions to type I interferon (IFN), an innate immune cytokine aberrantly elicited by {beta} amyloid plaques, and examine their role in cognition and neuropathology relevant to AD in a murine amyloidosis model. Long-term blockade of IFN receptor rescued both memory and synaptic deficits, and also resulted in reduced microgliosis, inflammation, and neuritic pathology. Interestingly, microglia-specific IFN receptor ablation attenuated the loss of post-synaptic terminals, whereas IFN signaling in neural cells contributed to pre-synaptic alteration and plaque accumulation. Intriguingly, IFN pathway activation displayed a strong inverse correlation with cognitive performance, promoting selective synapse engulfment by microglia rather than amyloid plaques. Overall, IFN signaling represents a critical module within the neuroinflammatory network of AD and prompts a concerted cellular state that is detrimental to memory and cognition.

neuroscience↗

bioRxiv2021

Pathogenic tau accelerates aging-associated activation of transposable elements in the mouse central nervous system

Transposable elements comprise almost half of the mammalian genome. A growing body of evidence suggests that transposable element dysregulation accompanies brain aging and neurodegenerative disorders, and that transposable element activation is neurotoxic. Recent studies have identified links between pathogenic forms of tau, a protein that accumulates in Alzheimer disease and related tauopathies, and transposable element-induced neurotoxicity. Starting with transcriptomic analyses, we find that age- and tau-induced transposable element activation occurs in the mouse brain. Among transposable elements that are activated at the RNA level in the context of brain aging and tauopathy, we find that the endogenous retrovirus (ERV) class of retrotransposons is particularly enriched. We show that protein encoded by Intracisternal A-particle, a highly active mouse ERV, is elevated in brains of tau transgenic mice. We further demonstrate that brains of tau transgenic mice contain increased DNA copy number of transposable elements, raising the possibility that these elements actively retrotranspose in the context of tauopathy. Taken together, our study lays the groundwork for future mechanistic studies focused on transposable element regulation in the aging mouse brain and in mouse models of tauopathy, while providing support for therapeutic approaches targeting transposable element activation for Alzheimer disease and related tauopathies.

neuroscience↗