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Biology subjects

Cohen, L. B.

Publications and source records attributed to Cohen, L. B..

12 recordsLinked to original sources

A genome-wide survey reveals a diverse array of enhancers coordinate the Drosophila innate immune response

To defend against microbes, animals regulate a complex immune response. The Drosophila innate immune system deploys a large transcriptional induction of signaling proteins, anti-microbial effectors, and other critical immune factors. This transcriptional response is encoded in enhancers, cis-regulatory sequences that modulate gene expression by binding transcription factors (TFs). While enhancers and transcription factor binding sites (TFBS) have been identified for several immune responsive genes in Drosophila, most enhancers that regulate immune-induced genes are unknown. By identifying enhancers, we can understand how their composition controls expression and contributes to infection outcome. We employed STARR-seq (Self Transcribing Active Regulatory-Region sequencing) in a hemocyte-like cell line to identify immune-specific enhancers across the D. melanogaster genome and performed ATAC-seq in hemocytes extracted from adult flies to assess the chromatin state of these enhancers before and after immune stimulus. We identified thousands of enhancers responsive to IMD stimulation, one of the two primary immune signaling pathways in Drosophila. As expected, immune enhancers are enriched for motifs of Relish, an NF-{kappa}B factor, and Kay/Jra, a bZip heterodimer pair, involved in the Imd and JNK pathways respectively, compared to enhancers active in unstimulated cells. However, when grouping enhancers by their target genes expression timing or functional role or by the enhancers chromatin accessibility pre- or post-stimulus, different groups of TFBS motifs are enriched, suggesting distinct regulatory logic for different parts of the immune response. Identification and characterization of the diverse array of enhancers that regulate the innate immune response expands our understanding of how animals fight infections.

genomics↗

Comparison of Activities of Transcription Factor NF-κB from Two Jellyfish Models

Herein, transcription factor Nuclear Factor-kappaB (NF-{kappa}B) is characterized as the downstream effector of putative innate immune signaling pathways from two model jellyfish, Aurelia aurita (Aa) and Clytia hemisphaerica (Ch). Both jellyfish NF-{kappa}B proteins consist primarily of the N-terminal DNA-binding/dimerization domain, and they lack the C-terminal ankyrin repeat inhibitory domain found in vertebrate NF-{kappa}B proteins. Both jellyfish NF-{kappa}B proteins bind to a consensus mammalian NF-{kappa}B binding site, and their AlphaFold3-predicted structures on DNA are similar to that of mouse NF-{kappa}B p50. Neither Aa- nor Ch-NF-{kappa}B activated transcription of an NF-{kappa}B-site reporter gene in human cells; however, Aa-NF-{kappa}B did activate transcription from a GAL4-site reporter gene in yeast, whereas Ch-NF-{kappa}B did not. Aa- and Ch-NF-{kappa}B were both constitutively located in the nucleus when expressed in vertebrate cells. Homologs of I{kappa}B-like proteins from both species interacted with their corresponding NF-{kappa}B proteins in co-immunoprecipitation assays in HEK 293T cells. These I{kappa}B-like proteins influenced the subcellular localization of their cognate NF-{kappa}B proteins in vertebrate cells, and their ankyrin repeat domains were predicted to interact with Ch-NF-{kappa}B in a manner similar to mammalian I{kappa}B and NF-{kappa}B. RNA-sequencing data from Ch animals indicate that Ch-NF-{kappa}B is expressed at high levels in early developmental stages, when Ch-I{kappa}B expression is low, suggesting that active Ch-NF-{kappa}B controls an early developmental process. In contrast, in adult animals the expression of Ch-I{kappa}B is high, suggesting that Ch-NF-{kappa}B requires a signal in order to become active. Overall, these results provide comparative information on the structure, activity, and mRNA expression of jellyfish NF-{kappa}B pathway proteins among jellyfish, and they suggest roles for NF-{kappa}B in developing and adult jellyfish.

molecular biology↗

Synaptic and Somatic Targeting of ArcLight, a Genetically Encoded Voltage Indicator

Voltage signals in neurons are highly compartmentalized, which can influence their specific functions within neuronal circuits. Targeting of a genetically encoded voltage indicator (GEVI) to specific subcellular compartments can enhance the signal-to-noise ratio and provide more precise information about the location and timing of synaptic firing across different neuronal regions, reducing spatiotemporal signal convolution. To achieve subcellular targeting of the GEVI, ArcLight, we utilized five different postsynaptic targeting sequences (Shaker K+ channel C-terminus, stargazin C-terminus, rat Neuroligin-1 C-terminus, and anti-homer1 nanobodies HC20 & HC87) to direct ArcLight expression to the excitatory postsynaptic density. Additionally, we assessed a presynaptic-targeting tag (rat Neurexin-1{beta} C-terminus) and a somatodendritic targeting tag (Kv2.1-Lk-Tlcn C-terminus). Patch clamp experiments in HEK293 cells showed that the targeting tags used in this study did not significantly alter ArcLights voltage sensitivity compared to controls. AAV infection in the mouse olfactory bulb demonstrated that the subcellular targeting sequences effectively localized GEVI expression to specific compartments of mitral/tufted cells, including postsynaptic densities, presynaptic terminals, and somatodendritic regions. Furthermore, in vivo voltage imaging in mice expressing targeting-enhanced ArcLight variants revealed odorant-evoked responses similar to those observed with the original ArcLight. This indicates that subcellular targeting did not significantly impact the voltage sensing capability of ArcLight in mitral/tufted cells.

neuroscience↗

Configural behavior response to a two component odor mixture

Configural odors are mixtures of odorant molecules that are perceived as an odor distinct from the components. They provide an attractive target for investigations of odor perception in the olfactory bulb. We investigated the perception of octanal and citronellal in mice using a Go/No-Go behavioral paradigm, and show that mice trained on the mixture of the two odorants respond selectively to the mixture, but not to the components delivered separately.

physiology↗

The olfactory bulb carries out concentration invariance calculations by itself and does it very quickly.

The olfactory bulb is known to carry out computations for the olfactory perception of concentration invariance of odor recognition, a perception that is essential for life as we know it. However it is not known whether these computations require the extensive feedback to the bulb from the many brain regions which send this feedback. We have measured the concentration dependence of the mitral cell output of the bulb before and after blocking this feedback by lidocaine infusion into the medial olfactory peduncle. Surprisingly we found that the concentration dependence of the mitral cell output was unaffected by the lidocaine block of feedback. Furthermore the computation is rapid; it is complete within a single 250 msec inhalation. The computations for concentration invariance are most likely carried out within the olfactory bulb itself and they are carried out quickly.

neuroscience↗

Amplification of Olfactory Signals by Anoctamin 9 is Essential for Mammalian Olfaction: a Risk Factor for the Covid-19-associated Anosmia

Sensing smells of foods, prey, or predators determines animal survival. Olfactory sensory neurons in the olfactory epithelium (OE) detect odorants, where cAMP and Ca2+ play a significant role in transducing odorant inputs to electrical activity. Here we show Anoctamin 9, a cation channel activated by cAMP/PKA pathway, is expressed in the OE and amplifies olfactory signals. Ano9- deficient mice had reduced olfactory behavioral sensitivity, electro-olfactogram signals, and neural activity in the olfactory bulb. In line with the difference in olfaction between birds and other vertebrates, chick ANO9 failed to respond to odorants, whereas chick CNGA2, a major transduction channel, showed greater responses to cAMP. Importantly, single-cell transcriptome data from Covid-19 patients revealed that Ano9 transcripts were markedly suppressed among genes in the olfactory signal pathway. The signal amplification by ANO9 is essential for mammalian olfactory transduction, whose downregulation may be a risk factor for the olfactory dysfunction in Covid-19 patients.

cell biology↗

The predicted bZIP transcription factor ZIP-1 promotes resistance to intracellular infection in Caenorhabditis elegans

Defense against intracellular infection has been extensively studied in vertebrate hosts, but less is known about invertebrate hosts. For example, almost nothing is known about the transcription factors that induce defense against intracellular intestinal infection in the model nematode Caenorhabditis elegans. Two types of intracellular pathogens that naturally infect the C. elegans intestine are the Orsay virus, which is a positive-sense RNA virus, and microsporidia, which are fungal pathogens. Surprisingly, these molecularly distinct pathogens induce a common host transcriptional response called the Intracellular Pathogen Response (IPR). Here we describe zip-1 as an IPR regulator that functions downstream of all known IPR activating and regulatory pathways. zip-1 encodes a putative bZIP transcription factor of previously unknown function, and we show how zip-1 controls induction of a subset of genes upon IPR activation. ZIP-1 protein is expressed in the nuclei of intestinal cells, and is required in the intestine to upregulate IPR gene expression. Importantly, zip-1 promotes resistance to infection by the Orsay virus and by microsporidia in intestinal cells. Altogether, our results indicate that zip-1 represents a central hub for all triggers of the IPR, and that this transcription factor plays a protective role against intracellular pathogen infection in C. elegans.

immunology↗

The Drosophila Baramicin polypeptide gene protects against fungal infection

The fruit fly Drososphila melanogaster combats microbial infection by producing a battery of effector peptides that are secreted into the haemolymph. Technical difficulties prevented the investigation of these short effector genes until the recent advent of the CRISPR/CAS era. As a consequence, many putative immune effectors remain to be characterized and exactly how each of these effectors contributes to survival is not well characterized. Here we describe a novel Drosophila antifungal peptide gene that we name Baramicin A. We show that BaraA encodes a precursor protein cleaved into multiple peptides via furin cleavage sites. BaraA is strongly immune-induced in the fat body downstream of the Toll pathway, but also exhibits expression in the nervous system. Importantly, we show that flies lacking BaraA are viable but susceptible to the enomopathogenic fungus Beauveria bassiana. Consistent with BaraA being directly antimicrobial, overexpression of BaraA promotes resistance to fungi and the IM10-like peptides produced by BaraA synergistically inhibit growth of fungi in vitro when combined with a membrane-disrupting antifungal. Surprisingly, BaraA males but not females display an erect wing phenotype upon infection. Collectively, we identify a new antifungal immune effector downstream of Toll signalling, improving our knowledge of the Drosophila antimicrobial response.

immunology↗

Conserved amino acids residing outside the voltage field can shift the voltage sensitivity and increase the signal size of Ciona based GEVIs

To identify potential regions of the voltage-sensing domain that could shift the voltage sensitivity of Ciona intestinalis based Genetically Encoded Voltage Indicators (GEVIs), we aligned 183 voltage-gated sodium channels from different organisms. Conserved polar residues were identified at multiple transmembrane loop junctions in the voltage sensing domain. Similar conservation of polar amino acids was found in the voltage sensing domain of the voltage-sensing phosphatase gene family. These conserved residues were mutated to nonpolar or oppositely charged amino acids in a GEVI that utilizes the voltage sensing domain of the voltage sensing phosphatase from Ciona fused to the fluorescent protein, super ecliptic pHlorin (A227D). Different mutations shifted the voltage sensitivity in a more positive or a more negative direction. Double mutants were then created by selecting constructs that shifted the optical signal to more negative potentials resulting in an improved signal in the physiological voltage range. The combination of two mutations, Y172A (intracellular loop between transmembrane segments S2 and S3) and D204K (extracellular loop between transmembrane segments S3 and S4) showed the increased the signal size from 2.5% to 13.8% for a 100 mV depolarization. Introduction of these mutations into previously developed GEVIs improved the dynamic range to 40% {Delta}F/F/100 mV.

neuroscience↗

Voltage imaging using transgenic mouse lines expressing the GEVI ArcLight in two olfactory cell types

Genetically encoded voltage indicators (GEVIs) allow for cell-specific optical recordings of membrane potential changes in defined cell populations. One tool that would further their use in the in vivo mammalian brain is transgenic reporter animals that facilitate precise and repeatable targeting with high expression levels. The present literature on the development and use of transgenic mouse lines as vehicles for GEVI expression is limited. Here we report the first in vivo experiments using a transgenic reporter mouse for the GEVI ArcLight (Ai86(TITL-ArcLight)), which utilizes a Cre/tTA dependent expression system (TIGRE 1.0). Following pairing to appropriate Cre- and tTA transgenic mice, we report two mouse lines with ArcLight expression restricted to olfactory sensory neurons (OMP-ArcLight), and a subpopulation of interneurons that include periglomerular and granule cells (Emx1-ArcLight) in the olfactory bulb (OB). The ArcLight expression in these lines was sufficient for in vivo imaging of odorant responses in single trials. Odor responses were measured in the OB using epifluorescence and 2-photon imaging. The voltage responses were odor-specific and concentration-dependent, and confirmed earlier conclusions from calcium measurements. This study shows that the ArcLight Ai86(TITL-ArcLight) transgenic line is a flexible genetic tool that can be used to record neuronal electrical activity of a variety of cell types with a signal-to-noise ratio that is comparable to previous reports using viral transduction.

neuroscience↗

The olfactory bulb contributes to the adaptation of odor responses: the input-output transformation

While humans and other animals exhibit adaptation to odorants, the neural mechanisms involved in this process are incompletely understood. One possibility is that it primarily occurs as a result of the interactions between odorants and odorant receptors expressed on the olfactory sensory neurons in the olfactory epithelium. In this scenario, adaptation would arise as a peripheral phenomenon transmitted into the brain. An alternative possibility is that adaptation occurs as a result of processing in the brain. Here we asked whether the olfactory bulb, the first stage of olfactory information processing in the brain, is involved in perceptual adaptation. Multicolor imaging was used to simultaneously measure the olfactory receptor nerve terminals (input) and mitral/tufted cell apical dendrites (output) that innervate the olfactory bulb glomerular layer. Repeated odor stimulation of the same concentration resulted in a decline in the output maps, while the input remained relatively stable. The results indicate that the mammalian olfactory bulb participates in olfactory adaptation.

neuroscience↗

Genetic, morphometric, and molecular analyses of interspecies differences in head shape and hybrid developmental defects in the wasp genus Nasonia

Males in the parasitoid wasp genus Nasonia (N. vitripennis, N. giraulti, N. longicornis) have distinct, species specific, head shapes. Fertile hybrids among the species are readily produced in the lab allowing genetic analysis of the evolved differences. In addition, the obligate haploidy of males makes these wasps a uniquely powerful model for analyzing the role of complex gene interactions in development and evolution. Previous analyses have shown that complex gene interactions underpin different aspects of the shape differences, and developmental incompatibilities that are specific to the head in F2 haploid hybrid males are also governed by networks of gene interaction. Here we use the genetic tools available in Nasonia to extend our understanding of the gene interactions that affect development and morphogenesis in male heads. Using artificial diploid male hybrids, we show that alleles affecting head shape are codominant, leading to uniform, averaged hybrid F1 diploid male heads, while the alleles mediating developmental defects are recessive, and are not visible in the diploid hybrids. We also determine that divergence in time, rather than in morphological disparity is the primary driver of hybrid developmental defects. In addition, we show that doublesex is necessary for the male head shape differences, but is not the only important factor. Finally we demonstrate that we can dissect complex interspecies gene interaction networks using introgression in this system. These advances represent significant progress in the complex web of gene interactions that govern morphological development, and chart the connections between genomic and phenotypic variation.

evolutionary biology↗