Biology subjects

Hernandez, G.

Publications and source records attributed to Hernandez, G..

At least 19 recordsLinked to original sources

bioRxiv2026

Bacteriophage Sf14 survival under simulated gastrointestinal conditions

Shigella flexneri is an enteric pathogen responsible for causing shigellosis, a type of bacillary dysentery of significant global health concern. The increasing prevalence of antibiotic resistance has driven the search for alternative treatments, including bacteriophage (phage) therapy. However, the effectiveness of orally administered phages for enteric pathogens depends on their ability to survive passage through the gastrointestinal tract. In this study, the ability of bacteriophage Sf14 to maintain infectivity was evaluated under simulated gastrointestinal conditions using a modified INFOGEST 2.0 in vitro digestion model. This model includes salivary, gastric, and intestinal fluids with physiologically relevant compositions of electrolytes, bile salts, and enzymes. Phages were incubated in each simulated phase at standard physiological temperature, then tested for infectivity using quantitative plaque assays. Results show that Sf14 remained stable during the short duration of the oral phase and for the duration of the intestinal phase. By contrast, survival in simulated gastric fluid required a pH of 2.75 or higher, with rapid and substantial loss of infectivity at pH 2.5 and below. These findings demonstrate that while Sf14 is stable in oral and intestinal environments, the gastric phase poses a critical barrier to phage survival. With in vivo fasting gastric pH ranging from 1.5 to 3, encapsulation would enable the most flexible oral phage therapy against enteric pathogens, but ingestion after eating or alongside antacids may be sufficient.

microbiology↗

bioRxiv2026

Anti-amyloid immunotherapy drives APOE4 specific increases in glial reactivity, perivascular immune activation, and ARIA-like events

Anti-amyloid antibodies represent the first disease modifying therapeutics for Alzheimers disease (AD). Adoption of these novel treatments has been slowed by the occurrence of amyloid related imaging abnormalities (ARIA) - treatment-associated edema (ARIA-E) or microhemorrhages (ARIA-H) that disproportionately affect carriers of the E4 allele of apolipoprotein E (APOE). With E4 carriers comprising nearly 70% of the AD population, there is a critical need to understand the unique vulnerability of E4 carriers to these events. To address this gap, we utilized the EFAD mouse model - which expresses human APOE isoforms on the 5xFAD background of amyloidosis - to directly compare the effects of anti-amyloid therapy across APOE genotypes. 9-month-old E2, E3, and E4FAD mice received weekly injections of chimeric Aducanumab (chAdu) or IgG control for 12 weeks, to assess APOE isoform-specific effects on amyloid dynamics, ARIA-H-like microhemorrhages, and underlying cellular and transcriptomic responses. E4FAD mice demonstrated plaque reductions with accompanying increases in microhemorrhages (measured on both MRI and histology), and increases in microglial and astrocyte reactivity - especially in the perivascular compartment. Additionally, vascular branching analysis and parallel single cell and spatial transcriptomics revealed a loss of vascular plasticity and increased inflammatory and immune signaling in the neurovascular units of E4FAD mice. Together, these findings suggest the cerebrovasculature of E4s is uniquely susceptible to antibody mediated vascular damage and provide immunological targets for the assessment or mitigation of ARIA risk in this highest need population

neuroscience↗

bioRxiv2026

Hierarchical cross-linking of a bacterial spore coat Hub protein

Hub proteins are highly connected nodes in protein-protein interaction networks and are often intrinsically disordered proteins (IDPs) or contain intrinsically disordered regions. In Bacillus subtilis, the morphogenesis of the spore surface is orchestrated by a set of so-called morphogenetic proteins that guide the assembly of distinct layers. Formation of the inner coat is directed by SafAFL and its shorter isoform, C30. Both are expressed early in sporulation under the control of {sigma}E and localize at the interface between the developing inner coat and the underlying cortex peptidoglycan. From this site, they act as organizational hubs, recruiting client proteins essential for coat maturation. Among these is Tgl, a transglutaminase synthesized later in development following activation of {sigma}K after engulfment completion. We show that the C30 domain exhibits IDP-like features yet self-assembles into >1200 kDa complexes stabilized by disulfide bonds and that these bonds are required for subsequent proper Tgl-mediated "spotwelding" cross-linking. Small-angle X-ray scattering (SAXS) and photobleaching show that Tgl immobilizes but does not drastically alter these assemblies. These findings support a hierarchical, biphasic model for inner coat assembly: initial self-assembly and disulfide stabilization, followed by Tgl-mediated cross-linking and structural stabilization. According to this model, the forms of SafAFL/C30 that dominate the two stages recruit different client proteins in register with the course of morphogenesis.

microbiology↗

bioRxiv2025

Coordinated overexpression of miR398 and miR408 confers broad-spectrum abiotic stress tolerance in melon.

MicroRNAs (miRNAs) in general and miR398 and miR408 in particular, have emerged as key regulators of plant adaptation to individual stress, yet their roles regulating the crop response to diverse unfavorable environments remain poorly explored. Here, we present the first melon (Cucumis melo) plants overexpressing miR398 and miR408 precursors, two conserved miRNAs involved in the regulation of cooper (Cu) homeostasis and associated with stress-response. Engineered plants exhibited enhanced vegetative development, including stem elongation, internode formation, root architecture, and leaf production. The significant increased accumulation of well-processed miR398 and miR408, along with the downregulation of their respective targets (Copper/Zinc Superoxide Dismutase and Basic Blue Protein) demonstrating the functional activity of the transgenes. Sequencing analysis revealed positive correlation in accumulation of miR398 and miR408, suggesting a previously undescribed form of coordinated miRNA regulation, potentially independent of conventional transcription factor activity. Transgenic plants showed improved tolerance to drought, salinity, heat, and cold stress, validating the role of miR398 and miR408 as master regulators of abiotic stress resilience in melon. This work highlights the potential of biotechnological strategies based on engineering Cu-related miRNAs to enhance crop performance under different adverse environments, thereby contributing to agricultural sustainability in the face of climate change.

plant biology↗

bioRxiv2025

Imp, a key regulator of transposable elements, cell growth, and differentiation genes during embryogenesis

Imps are a highly conserved family of RNA-binding proteins involved in embryonic development, cancer progression, and neurogenesis. However, the molecular pathways and RNAs regulated by Imp to control these processes remain poorly understood. Embryos derived from Imp mutant germline clones arrest development, and transcriptome analysis revealed significant dysregulation of genes involved in cell growth, differentiation, tube morphogenesis, neuronal projection development, and RNA metabolism, along with de-repression of transposable element (TE) RNAs. Consistent with these findings, Imp mutant embryos display TE-overexpression phenotypes, are smaller in size, and exhibit defective organ development, including impaired tracheal branching and gastrulation. Reduced levels of Imp at the larval neuromuscular junction (NMJ) impair synaptic bouton formation and decrease adult longevity. RIP-seq experiments showed that Imp-associated RNAs are enriched for TE RNAs. Proteomic analyses confirmed that several TE-encoded proteins are upregulated in Imp mutant embryos. Specifically, the Ty1 family retrotransposon Copia was derepressed. Consistent with recent findings that Copia is a potent inhibitor of synaptogenesis, its upregulation likely contributes to the impaired NMJ formation and broader embryonic defects observed in Imp mutants. Moreover, Imp associates with piRNA pathway proteins, ensures Piwi nuclear localization, and--like piwi mutants--its loss disrupts TE silencing and causes position-effect variegation (PEV) defects. The analysis of Imp complexes further points to potential mechanisms by which Imp may regulate TE expression. Overall, these results indicate that Imp maintains genome stability and ensures proper developmental progression and neuronal activity by regulating post-transcriptional processes and suppressing transposons.

developmental biology↗

bioRxiv2025

Evolution of increased longevity and slowed ageing in a genus of tropical butterfly

Evolution has given rise to lifespans in extant species ranging from days to centuries. Given that mechanisms of ageing are highly conserved, studying long-lived lineages across the animal kingdom could yield insights relevant for healthy ageing in humans. However, typical models of extended lifespan often live for decades, making them impractical for longitudinal studies. Ideal model systems would be organisms that are naturally long-lived compared to their close relatives, but have lifespans on experimentally tractable scales. Here, we present the Neotropical butterfly genus Heliconius as a novel model system for the evolution of extended longevity. We collate data from 27 species across the Heliconiini tribe to reveal a 25-fold variation in lifespan within the group, with our 348-day maximum for Heliconius hewitsoni longer than any butterfly species previously recorded in the scientific literature. While previous work has attributed this lifespan extension to a plastic response to enhanced nutrition, we conduct detailed survival and functional senescence analyses on two species representative of shorter- and longer-lived clades to show evidence of evolved, heritable mechanisms of slowed ageing in Heliconius. Our results add a new case study to the canon of noteworthy agers, and provide valuable insights into the evolution of increased longevity.

evolutionary biology↗

bioRxiv2025

The Crunchometer: A Low-Cost, Open-Source Acoustic Analysis of Feeding Microstructure

Elucidating the neuronal circuits that govern appetite requires precise, high-resolution monitoring of the microstructure of solid food consumption, a need unmet by existing tools, which are either costly or lack the temporal resolution to align feeding events with neuronal activity. To overcome this, we developed the Crunchometer, a low-cost, open-source acoustic system that uses computational algorithms to generate high-resolution feeding ethograms from the sounds produced during solid food consumption. Validation across energy states (hunger/satiety) confirmed its sensitivity to changes in feeding microstructure, and the system reliably detected semaglutide-induced suppression of intake and reduced preference for a high-fat diet. Leveraging its seamless integration with in vivo recordings in freely behaving mice, we paired the Crunchometer with lateral hypothalamus (LH) electrophysiology to identify "meal-related" neurons that track entire meals rather than individual bouts. Calcium imaging further revealed that distinct subsets of LH GABAergic and glutamatergic neurons were tuned to feeding only, to licking only, or to both behaviors. Thus, LH neuronal ensembles differentially encode the consumption of solid food versus liquid sucrose. These findings demonstrate that the Crunchometer is a robust, accessible platform for dissecting the neural correlates of feeding behavior at the resolution of a single bite. Significance statementThe Crunchometer is a low-cost, open-source technology that democratizes feeding analysis, enabling the precise dissection of neuronal circuits involved in appetite to advance therapies for obesity and eating disorders.

neuroscience↗

bioRxiv2025

PCSK9 dependent cholesterol acquisition and utilization underlies metastatic organ preference in pancreatic cancer.

To grow at distant sites, metastatic cells must overcome major challenges posed by the unique cellular and metabolic composition of secondary organs1. Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease that metastasizes to the liver and lungs. Despite evidence of metabolic reprogramming away from the primary site, the key drivers that dictate the ability of PDAC cells to colonize the liver or lungs and survive there are undefined. We identified Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) as predictive of colonization of the liver versus lungs by integrating datasets describing the metastatic tropism of human PDAC cell lines2, with in vivo metastasis modeling in mice and gene expression correlation analysis. PCSK9 is a negative regulator of low density lipoprotein(LDL)-cholesterol import and, accordingly, PCSK9-low PDAC cells exhibit strong preference for colonizing LDL-rich liver tissue. Cholesterol taken up by liveravid PCSK9-low cells is converted into the signaling oxysterol, 24(S)-hydroxycholesterol, which reprograms the surrounding microenvironment to induce nutrient release from neighboring hepatocytes. Conversely, PCSK9-high, lung-avid PDAC cells rely on transcriptional upregulation of the distal cholesterol synthesis pathway to generate intermediates, chiefly, 7dehydrodesmosterol and 7-dehydrocholesterol, with protective action against ferroptosis, a vulnerability in the oxygen-rich microenvironment of the lung. Increasing PCSK9 levels redirected liver-avid cells to the lung whereas its ablation drove lung-avid cells to the liver, thereby establishing PCSK9 as necessary and sufficient for secondary organ site preference. Our studies reveal PCSK9-driven differential utilization of the distal cholesterol synthesis pathway as a key and potentially actionable driver of metastatic growth in PDAC.

cancer biology↗

bioRxiv2025

Amphetamine in Adolescence Induces a Sex-Specific Mesolimbic Dopamine Phenotype in the Adult Prefrontal Cortex

Drugs of abuse in adolescence impact brain maturation and increase psychiatric risk, with differences in sensitivity between males and females. Amphetamine in adolescent male, but not female mice, causes dopamine axons intended to innervate the nucleus accumbens and to grow ectopically to the prefrontal cortex (PFC). This is mediated by drug-induced downregulation of the Netrin-1 receptor DCC. How off-target dopamine axons function in the adult PFC remains to be determined. Here we report that males and females show place preference for amphetamine in adolescence. However, only in males, amphetamine increases PFC dopamine transporter expression in adulthood: leading to aberrant baseline dopamine transients, faster dopamine release, and exaggerated responses to acute methylphenidate. Upregulation of DCC in adolescence, using CRISPRa, prevents all these changes. Mesolimbic dopamine axons rerouted to the PFC in adolescence retain anatomical and functional phenotypes of their intended target, rendering males enduringly vulnerable to the harmful effects of drugs of abuse.

neuroscience↗

bioRxiv2024

Leucine Aminopeptidase LyLAP enables lysosomal degradation of membrane proteins

Proteolysis of hydrophobic helices is required for complete breakdown of every transmembrane protein trafficked to the lysosome and sustains high rates of endocytosis. However, the lysosomal mechanisms for degrading hydrophobic domains remain unknown. Combining lysosomal proteomics with functional genomic data mining, we identify Lysosomal Leucine Aminopeptidase (LyLAP; formerly Phospholipase B Domain-Containing 1) as the hydrolase most tightly associated with elevated endocytic activity. Untargeted metabolomics and biochemical reconstitution demonstrate that LyLAP is not a phospholipase, but a processive monoaminopeptidase with strong preference for N-terminal leucine - an activity necessary and sufficient for breakdown of hydrophobic transmembrane domains. LyLAP is upregulated in pancreatic ductal adenocarcinoma (PDA), which relies on macropinocytosis for nutrient uptake, and its ablation led to buildup of undigested hydrophobic peptides, which compromised lysosomal membrane integrity and inhibited PDA cell growth. Thus, LyLAP enables lysosomal degradation of membrane proteins, and may represent a vulnerability in highly endocytic cancer cells. One sentence summaryLyLAP degrades transmembrane proteins to sustain high endocytosis and lysosomal membrane stability in pancreatic cancer.

biochemistry↗

bioRxiv2024

Covalent inhibition of the SARS-CoV-2 NiRAN domain via an active-site cysteine

The kinase-like NiRAN domain of nsp12 in SARS-CoV-2 catalyzes the formation of the 5 RNA cap structure. This activity is required for viral replication, offering a new target for the development of antivirals. Here, we develop a high-throughput assay to screen for small molecule inhibitors targeting the SARS-CoV-2 NiRAN domain. We identified NCI-2, a compound with a reactive chloromethyl group that covalently binds to an active site cysteine (Cys53) in the NiRAN domain, inhibiting its activity. NCI-2 can enter cells, bind to, and inactivate ectopically expressed nsp12. A cryo-EM reconstruction of the SARS-CoV-2 replication-transcription complex (RTC) bound to NCI-2 offers a detailed structural blueprint for rational drug design. Although NCI-2 showed limited potency against SARS-CoV-2 replication in cells, our work lays the groundwork for developing more potent and selective inhibitors targeting the NiRAN domain. This approach presents a promising therapeutic strategy for effectively combating COVID-19 and potentially mitigating future coronavirus outbreaks.

biochemistry↗

bioRxiv2024

Automated cell tracking using 3D nnUnet and Light Sheet Microscopy to quantify regional deformation in zebrafish

Light Sheet Microscopy (LSM) in conjunction with embryonic zebrafish, is rapidly advancing three-dimensional, in vivo characterization of myocardial contractility. Preclinical cardiac deformation imaging is predominantly restricted to a low-order dimensionality image space (2i) or suffers from poor reproducibility. In this regard, LSM has enabled high throughput, non-invasive 4i (3d+time) characterization of dynamic organogenesis within the transparent zebrafish model. More importantly, LSM offers cellular resolution across large imaging Field-of-Views at millisecond camera frame rates, enabling single cell localization for global cardiac deformation analysis. However, manual labeling of cells within multilayered tissue is a time-consuming task and requires substantial expertise. In this study, we applied the 3i nnU-Net with Linear Assignment Problem (LAP) framework for automated segmentation and tracking of myocardial cells. Using binarized labels from the neural network, we quantified myocardial deformation of the zebrafish ventricle across 4-6 days post fertilization (dpf). Our study offers tremendous promise for developing highly scalable and disease-specific biomechanical quantification of myocardial microstructures.

bioengineering↗

bioRxiv2024

Functional screen for mediators of onco-mRNA translation specificity

Oncogenic protein dosage is tightly regulated to enable cancer cells to adapt and survive. Whether this is regulated at the level of translational control and the key factors in cis and trans remain unknown. The Myc oncogene is a central paradigm of an exquisitely regulated oncogene and a major driver of pancreatic ductal adenocarcinoma (PDAC). Using a functional genome-wide CRISPRi screen in PDAC cells, we identified activators of selective MYC translation through its 5 untranslated region (5UTR) and validated four RNA binding proteins (RBPs), including epitranscriptome modifiers. Among these RBPs, our top hit was RBM42, which is highly expressed in PDAC and predicts poor survival. Combining polysome sequencing and CLIP-seq analyses, we find that RBM42 binds and selectively regulates the translation of MYC and a precise, yet vital suite of pro-oncogenic transcripts, including JUN and EGFR. Mechanistically, employing IP-mass spectrometry analysis, we find that RMB42 is a novel ribosome-associated protein (RAP). Using DMS-Seq and mutagenesis analysis, we show that RBM42 directly binds and remodels the MYC 5UTR RNA structure, facilitating the formation of the translation pre-initiation complex. Importantly, RBM42 is necessary for human PDAC cell growth and fitness and PDAC tumorigenesis in xenograft mouse models in a Myc-dependent manner in vivo. In PDAC patient samples, RBM42 expression is correlated with Myc protein levels and transcriptional activity. This work transforms our understanding of the translational code in cancer and offers a new therapeutic opening to target the expression of oncogenes.

cancer biology↗

bioRxiv2024

Modality specific memory enhancement in Heliconius butterflies

How animals perceive, process and respond to environmental cues is tightly tuned to the species-specific demands, and reflected by the structure of neural systems. In the Neotropical butterflies, Heliconius, the mushroom bodies, insect learning and memory centres, are significantly expanded compared to their closest relatives. This expansion coincided with the evolution of a novel diet, pollen feeding, and a spatial foraging behaviour consistent with trap-lining. Previous research has shown that Heliconius have more accurate visual long-term memory than other Heliconiini. Here, we tested whether this enhanced memory stability is specific to visual cues by conducting a long-term olfactory memory assay in two Heliconius species and two outgroup species. We found no differences in the long-term olfactory memory between Heliconius species and the outgroup species. Combining data from olfactory and visual memory trials confirms a significant shift in performance among sensory modalities between Heliconius and outgroup genera. In contrast, tests of how Heliconiini prioritise olfactory and visual cues when in presented in conflict also show no consistent shift in attentiveness to sensory cues between species. Our data provide a rare case where memory performance has been compared across species and sensory modalities, to identify evidence of a modality specific shift.

animal behavior and cognition↗

bioRxiv2024

SYSTEMIC FRATAXIN DEFICIENCY CAUSES TISSUE-DEPENDENT IRON HOMEOSTASIS ALTERATIONS: IMPLICATIONS FOR FRIEDREICH ATAXIA

Friedreich Ataxia (FA) is a cardio-neurodegenerative disease caused by mutations in the frataxin gene, which result in low frataxin expression. It is well-established that frataxin deficiency affects iron homeostasis, but the tissue-specificity of these alterations is poorly understood. In this study, we have analyzed iron homeostasis alterations in the FXNI151F mouse model, which presents systemic frataxin deficiency and neurological defects resembling FA patients. Iron overload is observed in the brain from 21-week old FXNI151F mice, both males and females, and it does not further accumulate in older animals. It is also observed in livers from 39-week old mutant females, but not in males. Iron signaling is altered in all tissues: in brain and liver Iron Regulatory Protein 1 (IRP1) content is decreased, while in heart increased IRP2 and decreased specific aconitase 2 activity are observed. Remarkably, these cardiac alterations are partially restored in 39- week-old animals, suggesting that the heart is activating an iron-deficiency response to compensate for deficient iron-sulfur biogenesis. Our findings demonstrate that frataxin deficiency affects iron homeostasis in a time dependent and tissue-specific manner, and that the pathological mechanisms in FA comprise both iron accumulation and limited iron availability. Understanding this specificity is crucial for the design of iron-related therapeutic interventions aiming to improve FA symptomatology.

biochemistry↗

bioRxiv2024

Red harvester ant nests impact soil compaction but not temperature in peri-urban habitats of the Lower Rio Grande Valley

Ants are vital ecosystem engineers that can influence soil properties, subsequent soil processes, and associated biota via underground nest construction. Harvester ants consume seeds and are often found in arid areas, frequently altering soil chemistry and bulk density of the soils in and around their nest sites. Many species of harvester ants also intentionally remove vegetation around nest openings, creating cones or discs of bare soil that may further alter soil temperatures. However, much of the work investigating the impacts of harvester ants on soil properties has occurred in shrubland and grassland settings rather than suburban environments. We aimed to determine if Pogonomyrmex barbatus (Smith) (Hymenoptera: Formicidae) nests in a suburban habitat in the Lower Rio Grande Valley in Texas similarly altered soil properties. First, we measured active nest disc size to determine changes and colony persistence. Then we assessed soil compaction and surface temperature along a gradient centered on the disc. We found that disc size did not increase throughout the two-year observation period and that nests with smaller discs were less likely to persist between years. While we did not observe any changes in surface temperature across the gradient, we found a significant increase in soil compaction with greater distance from the center of the disc. These data indicate that increased nest size increases the extent of soil impacted. The impacts of nests reducing soil compaction, particularly within a suburban landscape with precipitation run-off issues and a highly disturbed plant community should be addressed in future studies.

ecology↗

bioRxiv2023

Multimodal identification of rare potent effector CD8 T cells in solid tumors

The anti-tumor function of CD8 T cells is limited through well-established pathways of T cell exhaustion (TEX). Strategies to capture emergent functional states amongst this dominant trajectory of dysfunction are necessary to find pathways to durable anti-tumor immunity. By leveraging transcriptional reporting (by the fluorescent protein TFP) of the T cell activation marker Cd69, related to upstream AP-1 transcription factors, we define a classifier for potent versus sub-optimal CD69+ activation states arising from T cell stimulation. In tumors, this delineation acts an additional functional readout along the TEX differentiation trajectory, within and across TEX subsets, marked by enhanced effector cytokine and granzyme B production. The more potent state remains differentially prominent in a T cell-mediated tumor clearance model, where they also show increased engagement in the microenvironment and are superior in tumor cell killing. Employing multimodal CITE-Seq in human head and neck tumors enables a similar strategy to identify Cd69RNAhiCD69+ cells that also have enhanced functional features in comparison to Cd69RNAloCD69+ cells, again within and across intratumoral CD8 T cell subsets. Refining the contours of the T cell functional landscape in tumors in this way paves the way for the identification of rare exceptional effectors, with imminent relevance to cancer treatment. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=120 SRC="FIGDIR/small/559470v2_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@4a9429org.highwire.dtl.DTLVardef@4535d9org.highwire.dtl.DTLVardef@1d26e03org.highwire.dtl.DTLVardef@34acd2_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

bioRxiv2023

Role of BicDR in bristle shaft construction, tracheal development, and support of BicD functions

Cell polarization requires asymmetric localization of numerous mRNAs, proteins, and organelles. The movement of cargo towards the minus end of microtubules mostly depends on cytoplasmic dynein motors, which function as multiprotein complexes. In the dynein/dynactin/Bicaudal-D (DDB) transport machinery, Bicaudal-D (BicD) links the cargo to the motor. Here we focus on the role of BicD-related (BicDR) and its contribution to microtubule-dependent transport processes. Drosophila BicDR is required for the normal development of bristles and dorsal trunk tracheae. Together with BicD, it contributes to the organization and stability of the actin cytoskeleton in the not-yet-chitinized bristle shaft and the localization of Spn-F and Rab6 at the distal tip. We show that BicDR supports the function of BicD in bristle development and our results suggest that BicDR transports cargo more locally whereas BicD is more responsible for delivering functional cargo over the long distance to the distal tip. We identified the proteins that interact with BicDR and appear to be BicDR cargo in embryonic tissues. For one of them, EF1{gamma}, we showed that EF1{gamma} genetically interacts with BicD and BicDR in the construction of the bristles.

cell biology↗