Biology subjects

Johnson, M. A.

Publications and source records attributed to Johnson, M. A..

At least 19 recordsLinked to original sources

bioRxiv2026

LAMA2-related muscular dystrophy alters Schwann cell calcium homeostasis and increases peripheral nerve inflammation

LAMA2-related muscular dystrophy (LAMA2-RD) affects skeletal muscle and peripheral nerves, yet the consequences of LAMA2 deficiency on peripheral nerve integrity beyond early postnatal development remain incompletely understood. We investigated sciatic nerve architecture and molecular alterations across postnatal life in hypomorphic Lama2dy2J/dy2J mice. LAMA2 localizes around the abaxonal surface of myelinating Schwann cells in control nerves. LAMA2-deficient nerves exhibited patchy regions lacking myelinated axons from early postnatal stages into adulthood, including expanded Remak bundles along with axons completely lacking normal Schwann cell ensheathment. In adult nerves, myelin infolding and reduced myelin circularity revealed abnormalities in the architecture of myelin that had formed. Bulk sciatic nerve RNA sequencing identified altered calcium-signaling and immune-related transcriptional signatures. Complementary Fura Red measurements in primary nerve-derived Schwann cell cultures demonstrated decreased intracellular calcium in LAMA2-deficient samples, while ATP-evoked responses were preserved. Older LAMA2-deficient nerves also exhibited increased CD45+CD11b+ myeloid-cell infiltration. Together, these observations extend the characterization of LAMA2-associated neuropathy into adulthood and identify calcium homeostasis and neuroimmune responses as candidate processes relevant to persistent peripheral nerve pathology.

neuroscience↗

bioRxiv2026

IL-10/ACOD1 axis regulates catabolism of phagocytosed lipids in trained macrophages

Macrophages clear excess host and microbial debris to restore homeostasis in inflamed tissues, yet the regulation and molecular fate of phagocytosed lipids during innate immune training remains largely unexplored. Leveraging stable isotope tracing of 13C-labeled bacteria, we establish an experimental framework to track microbe-to-host lipid transfer and define the fates of microbial lipids in macrophages in vitro and in vivo. While naive macrophages scavenge phagocytosed bacterial fatty acids into the host lipidome, TLR4-trained macrophages direct flux to mitochondria for {beta}-oxidation or lipid droplets in the context of mitochondrial dysfunction. While TLR4 signaling increases ACOD1 expression to produce itaconate that throttles TCA flux, trained macrophages produce IL-10 that reduces ACOD1 to sustain bacterial lipid disposal and promote resolution. These findings reveal an IL-10/ACOD1 regulatory axis in trained macrophages that reprograms lipid metabolism to optimally reestablish tissue homeostasis post-inflammation.

immunology↗

bioRxiv2026

The State of Motion: Demographic and representational consequences of motion-based exclusion in fMRI

Large-scale neuroimaging datasets are increasingly used to map relationships between brain structure, function, and behavior across the human lifespan. Routinely, analyses exclude participants who moved too much during imaging. While this decision is framed as quality control, it is increasingly recognized that head motion is not randomly distributed across individuals within a study, and so motion-based exclusion may preferentially remove people with particular characteristics relevant to the scientific goals of the study. Here we survey head motion and how it relates to participant characteristics across six large, publicly available datasets spanning nearly the entire human lifespan, namely the Human Connectome Project (HCP) Young Adult, HCP in Development, HCP in Aging, Adolescent Brain Cognitive DevelopmentSM Study, UK Biobank, and Spatial Topology project. These six datasets comprise more than 50,000 unique participants and 300,000 scans. We further benchmark our findings against motion distributions aggregated by MRIQC across more than 1.5 million scans. Under commonly applied strict exclusion thresholds, large fractions of participants would be removed (exceeding 80 % in the UK Biobank task data), and these removals were demographically structured, disproportionately excluding younger and older participants, those with higher BMI, and those with motion-associated clinical conditions. Respiratory pseudo-motion inflated estimates of head motion in adult cohorts, and applying notch filtering to remove respiratory frequencies from these estimates meaningfully reduced exclusion rates. Exclusion also carried downstream consequences. Strict thresholds reduced statistical power, inflated study costs, and altered the apparent predictability of behavioral phenotypes by removing a non-random, behaviorally distinct subgroup. These findings demonstrate that motion exclusion thresholds are not neutral quality-control decisions but structured selection mechanisms that reshape the composition of neuroimaging samples. We recommend that studies report the demographic characteristics of excluded participants, prefer data-driven censoring methods over fixed motion cutoffs, and clarify the target population while considering appropriate weighting techniques.

neuroscience↗

bioRxiv2026

The p97 adaptor p47/NSFL1C is necessary for stress granule dissolution after heat stress

Stress granules form in response to diverse cellular perturbations to sequester translation components until the stress is resolved. Stress granules are composed of RNA-protein assemblies in membrane delimited structures and must be rapidly disassembled to release components to allow translation to resume. Disassembly of stress granules formed in response to heat stress is dependent on ubiquitiylation of stress granule components such as G3BP1. Ubiquitylation of stress granule proteins recruits the AAA-ATPase p97 (also known as VCP) to enable ubiquitin-dependent disassembly of these structures. Loss of p97 activity leads to the persistence of stress granules and is implicated in several age-related neurodegenerative diseases. Here we show that p97 recruitment to stress granules is dependent on its ubiquitin binding co-factor p47. p47 translocates to stress granules in response to a variety of cellular stressors and is required for the recruitment of p97 to stress granules. Loss of p47 leads to an inhibition in stress granule disassembly. We further show that p47 associates with G3BP1 in response to heat stress in a ubiquitin-dependent manner. Taken together our data adds to the growing list of p97 adaptors that are implicated in the recruitment of p97 for dissolution of stress granules.

cell biology↗

bioRxiv2025

Targeting Galectin-3 to modulate inflammation in LAMA2-deficient congenital muscular dystrophy

LAMA2-deficient congenital muscular dystrophy (LAMA2-CMD) is a severe neuromuscular disorder characterized by muscle degeneration, chronic inflammation, and fibrosis. While inflammation is one the hallmarks of LAMA2-CMD, the immune cell composition in laminin-deficient muscles remains understudied. Consequently, targeted pharmacological intervention to reduce inflammation remains underexplored. Here, we characterized the immune landscape in the dyW mouse model of LAMA2-CMD using RNA sequencing and flow cytometry. Transcriptomic analysis of dyW quadriceps femoris muscle identified 2,143 differentially expressed genes, with most upregulated genes linked to immune-related pathways. Lgals3 (Galectin-3) was significantly upregulated and identified as a key upstream regulator of the immune-related pathways. Flow cytometry revealed elevated leukocyte (CD45) infiltration, with macrophages as the predominant population. Pro-inflammatory (M1) macrophages were increased, whereas anti-inflammatory (M2) macrophages remained low, indicating persistent and unresolved inflammation. Notably, Galectin-3+ macrophages were significantly enriched, suggesting that Galectin-3 drives inflammation in LAMA2-CMD. Treatment of dyW mice with TD-139, a Galectin-3 inhibitor, reduced leukocyte infiltration, decreased Galectin-3+ macrophages, and shifted macrophage polarization toward an M2 anti-inflammatory profile. RNA sequencing of TD-139-treated dyW muscles showed upregulation of muscle contraction pathways and downregulation of fibrosis-related genes. These findings highlight Galectin-3+ macrophages as key contributors to LAMA2-CMD pathophysiology and support further exploration of TD-139 as a potential therapeutic strategy for LAMA2-CMD and other dystrophic conditions driven by chronic inflammation.

immunology↗

bioRxiv2024

Image Processing in the Acute to Chronic Pain Signatures (A2CPS) Project

The Acute to Chronic Pain Signatures (A2CPS) project is a large-scale, multi-site initiative aimed at identifying biomarkers and biosignatures that predict the transition from acute to chronic pain. The project is collecting multimodal, longitudinal data from over 2,500 individuals at risk for developing chronic pain after surgery. Here we describe the neuroimaging component of A2CPS, including the acquisition protocols, processing pipelines, and contents of the initial data release. The imaging protocol includes structural, diffusion, resting-state and task-based functional magnetic resonance imaging (MRI) data. Data are collected across multiple clinical sites using different scanner manufacturers, with attention to protocol harmonization and quality control. The processing pipeline integrates several established neuroimaging tools to extract potential biomarkers, including measures of brain structure, connectivity, and pain-related neural signatures. The first data release includes pre-surgical imaging data for 595 participants, with high quality ratings across modalities (98.7% of sMRI, 99.8% of dMRI, and 94.6% of fMRI images were rated as acceptable or better). Initial analyses demonstrate expected relationships between brain-derived measures and clinical variables, such as associations between brain age and psychological factors. This dataset represents a valuable resource for both pain research and neuroimaging methods development, with future releases planned to include additional participants and expanded analysis pipelines and processed data derivatives.

neuroscience↗

bioRxiv2024

Contrasting Cognitive, Behavioral, and Physiological Responses to Breathwork vs. Naturalistic Stimuli in Reflective Chamber and VR Headset Environments

The MindGym, a novel immersive technology utilizing a reflective chamber environment, was developed to create standardized experiential content, including anxiolytic experiences. This study examined whether therapeutic experiences originally created in the MindGym could maintain their efficacy when delivered via 360-degree recordings through virtual reality (VR) headsets. A randomized controlled trial (N=126) compared anxiety reduction, cognitive performance, and physiological responses across four conditions: MindGym and VR platforms, each delivering either breathwork or rain stimuli. Results demonstrated significant improvements across all conditions in cognitive performance (Trail Making Test RTACC, p.fdr<.001; Architex Total Speed, p.fdr<.001) and anxiety reduction (STAI, p.fdr<.001). Breathwork conditions produced greater decreases in breath rate compared to rain stimuli (p.fdr=.002). Treatment responses were moderated by individual differences, with absorption (MODTAS) predicting both awe (p.fdr=.004) and ego dissolution (p.fdr=.015), while openness to experience interacted with stimuli type to influence anxiety reduction (p.fdr=.038). The anxiolytic effects originally generated in the MindGym maintained full efficacy when translated to VR delivery, with no significant differences in effectiveness or immersion between the original environment and its virtual reproduction. These findings establish the MindGym as a viable content creation platform for immersive, anxiety-reducing experiences that can be successfully adapted to more accessible delivery systems, while highlighting the potential for personalization based on individual differences. Future research should investigate the translation of more complex MindGym-generated experiences to expand accessible anxiety management tools.

neuroscience↗

bioRxiv2024

Enhanced pollen tube performance at high temperature contributes to thermotolerant fruit production in tomato.

Rising temperature extremes during critical reproductive periods threaten the yield of major grain and fruit crops. Flowering plant reproduction depends on development of sufficient numbers of pollen grains and on their ability to generate a cellular extension, the pollen tube, which elongates through the pistil to deliver sperm cells to female gametes for double fertilization. These critical phases of the life cycle are sensitive to temperature and limit productivity under high temperature (HT). Previous studies have investigated the effects of HT on pollen development, but little is known about how HT applied during the pollen tube growth phase affects fertility. Here, we used tomato as a model fruit crop to determine how HT affects the pollen tube growth phase, taking advantage of cultivars noted for fruit production in exceptionally hot growing seasons. We found that exposure to HT solely during the pollen tube growth phase limits fruit biomass and seed set more significantly in thermosensitive cultivars than in thermotolerant cultivars. Importantly, we found that pollen tubes from the thermotolerant Tamaulipas cultivar have enhanced growth in vivo and in vitro under HT. Analysis of the pollen tube transcriptomes response to HT allowed us to develop hypotheses for the molecular basis of cellular thermotolerance in the pollen tube and we define two response modes (enhanced induction of stress responses, and higher basal levels of growth pathways repressed by heat stress) associated with reproductive thermotolerance. Importantly, we define key components of the pollen tube stress response identifying enhanced ROS homeostasis and pollen tube callose synthesis and deposition as important components of reproductive thermotolerance in Tamaulipas. Our work identifies the pollen tube growth phase as a viable target to enhance reproductive thermotolerance and delineates key pathways that are altered in crop varieties capable of fruiting under HT conditions. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=95 SRC="FIGDIR/small/606234v1_ufig1.gif" ALT="Figure 1"> View larger version (35K): org.highwire.dtl.DTLVardef@25e5acorg.highwire.dtl.DTLVardef@98fb1org.highwire.dtl.DTLVardef@1b8b9cborg.highwire.dtl.DTLVardef@adcca4_HPS_FORMAT_FIGEXP M_FIG C_FIG

plant biology↗

bioRxiv2023

Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity

Dopaminergic neurons of the substantia nigra exist in a persistent state of vulnerability resulting from high baseline oxidative stress, high energy demand, and broad unmyelinated axonal arborizations. Impairments in the storage of dopamine compound this stress due to cytosolic reactions that transform the vital neurotransmitter into an endogenous neurotoxicant, and this toxicity is thought to contribute to the dopamine neuron degeneration that occurs Parkinsons disease. We have previously identified synaptic vesicle glycoprotein 2C (SV2C) as a modifier of vesicular dopamine function, demonstrating that genetic ablation of SV2C in mice results in decreased dopamine content and evoked dopamine release in the striatum. Here, we adapted a previously published in vitro assay utilizing false fluorescent neurotransmitter 206 (FFN206) to visualize how SV2C regulates vesicular dopamine dynamics and determined that SV2C promotes the uptake and retention of FFN206 within vesicles. In addition, we present data indicating that SV2C enhances the retention of dopamine in the vesicular compartment with radiolabeled dopamine in vesicles isolated from immortalized cells and from mouse brain. Further, we demonstrate that SV2C enhances the ability of vesicles to store the neurotoxicant 1-methyl-4-phenylpyridinium (MPP+) and that genetic ablation of SV2C results in enhanced 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced vulnerability in mice. Together, these findings suggest that SV2C functions to enhance vesicular storage of dopamine and neurotoxicants, and helps maintain the integrity of dopaminergic neurons.

neuroscience↗

bioRxiv2023

ALS-related p97 R155H mutation disrupts lysophagy in iPSC-derived motor neurons

Mutations in the AAA+ ATPase p97 (also known as valosin containing protein, VCP) cause multisystem proteinopathy 1 (MSP-1) which includes amyotrophic-lateral sclerosis (ALS); however, the pathogenic mechanisms that contribute to motor neuron loss in familial ALS caused by p97 mutations remain obscure. Here, we use two distinct induced pluripotent stem cell models differentiated into spinal motor neurons to investigate how p97 mutations perturb the motor neuron proteome. Using multiplexed quantitative proteomics in these cells, we find that motor neurons harboring the p97 R155H mutation have deficits in lysosome quality control and the selective autophagy of lysosomes (lysophagy). p97 R155H motor neurons are unable to efficiently clear damaged lysosomes and have reduced viability. Additionally, lysosomes in mutant motor neurons have increased pH compared to their wildtype counterparts. The endo-lysosomal damage repair (ELDR) complex is required for clearance of damaged lysosomes and involves UBXD1-p97 interaction which is disrupted in mutant motor neurons. Finally, we report that inhibition of the ATPase activity of p97 R155H using the ATP competitive inhibitor CB-5083 rescues lysophagy defects in mutant motor neurons. These results add to the increasing evidence that endo-lysosomal dysfunction is a key aspect of disease pathogenesis in p97-related disorders.

neuroscience↗

bioRxiv2023

CRISPRa-induced upregulation of human LAMA1 compensates for LAMA2-deficiency in Merosin-deficient congenital muscular dystrophy

Merosin-deficient congenital muscular dystrophy (MDC1A) is an autosomal recessive disorder caused by mutations in the LAMA2 gene, resulting in a defective form of the extracellular matrix protein laminin-2 (LAMA2). Individuals diagnosed with MDC1A exhibit progressive muscle wasting and declining neuromuscular functions. No treatments for this disorder are currently available. We previously showed that postnatal Lama1 upregulation, achieved through CRISPR activation (CRISPRa), compensates for Lama2 deficiency and prevents neuromuscular pathophysiology in a mouse model of MDC1A. In this study, we assessed the feasibility of upregulating human LAMA1 as a potential therapeutic strategy for individuals with MDC1A, regardless of their mutations. We hypothesized that CRISPRa-mediated upregulation of human LAMA1 would compensate for the lack of LAMA2 and rescue cellular abnormalities in MDC1A fibroblasts. Global transcriptomic and pathway enrichment analyses of fibroblasts collected from individuals carrying pathogenic LAMA2 mutations, compared with healthy controls, indicated higher expression of transcripts encoding proteins that contribute to wound healing, including Transforming Growth Factor-{beta} (TGF-{beta}) and Fibroblast Growth Factor (FGF). These findings were supported by wound-healing assays indicating that MDC1A fibroblasts migrated significantly more rapidly than the controls. Subsequently, we treated the MDC1A fibroblasts with SadCas9-2XVP64 and sgRNAs targeting the LAMA1 promoter. We observed robust LAMA1 expression, which was accompanied by significant decreases in cell migration and expression of FGFR2, TGF-{beta}2, and ACTA2, which are involved in the wound-healing mechanism in MDC1A fibroblasts. Collectively, our data suggest that CRISPRa-mediated LAMA1 upregulation may be a feasible mutation-independent therapeutic approach for MDC1A. This strategy might be adapted to address other neuromuscular diseases and inherited conditions in which strong compensatory mechanisms have been identified.

genetics↗

bioRxiv2022

Connexin36 expression in the cochlear nucleus complex of the echolocating bat, Eptesicus fuscus

Gap junctions and electrical synapses in the central nervous system are associated with rapid temporal processing and coincidence detection. Using histology, immunohistochemistry, and in situ hybridization, we investigated the distribution of Connexin36 (Cx36), a protein that comprises neuronal gap junctions, throughout the cochlear nucleus complex of the echolocating big brown bat, Eptesicus fuscus, a species exhibiting extreme behavioral sensitivity to minute temporal changes in ultrasonic echoes. For comparison, we visualized Cx36 expression in the cochlear nucleus of transgenic Cx36 reporter mice, species that hear ultrasound but do not echolocate. We observed Cx36 expression in the anteroventral and dorsal cochlear nucleus, with more limited expression in the posteroventral cochlear nucleus, of both species. Several different morphological cell types were labeled, including globular and spherical bushy, octopus, stellate, and fusiform cells. Labeled Cx36 puncta were also observed. Cx36 expression in the bat was spread throughout a relatively smaller area of the cochlear nucleus than in the mouse, even though the bat cochlear nucleus is hypertrophied. In the bat, the anteroventral cochlear nucleus showed higher percent area label than the dorsal cochlear nucleus, with a trend towards the opposite result in the mouse. The presence of gap junctions appears to be a conserved feature of the mammalian cochlear nucleus and thus not uniquely tied to the temporal hyperacuity of echolocation.

neuroscience↗

bioRxiv2021

A genome-edited β-cell model of Prader-Willi syndrome reveals chronic deficits in endoplasmic reticulum chaperones and insulin secretion

Prader-Willi syndrome (PWS) is a multisystem disorder with neurobehavioral, metabolic, and hormonal phenotypes, caused by loss of expression of a paternally-expressed imprinted gene cluster. Prior evidence from a PWS mouse model identified abnormal pancreatic islet development with retention of aged insulin and deficient insulin secretion. To determine the collective roles of PWS genes in {beta}-cell biology, we used genome-editing to generate isogenic, clonal INS-1 insulinoma lines having 3.16 Mb deletions of the silent, maternal (control) or active, paternal PWS-alleles. PWS {beta}-cells demonstrated a significant cell-autonomous reduction in basal and glucose-stimulated insulin secretion. Further, proteomic analyses revealed reduced levels of cellular and secreted hormones, including all insulin peptides and amylin, concomitant with reduction of at least ten endoplasmic reticulum (ER) chaperones, including GRP78 and GRP94. Critically, transcriptomic studies demonstrated that the broad reduction of ER chaperones originated from transcriptional downregulation without corresponding changes for Ins1 and Ins2. In contrast to the dosage compensation previously seen for ER chaperones in Grp78 or Grp94 gene knockouts or knockdown, compensation is precluded by the stress-independent deficiency of ER chaperones in PWS {beta}-cells. Consistent with reduced ER chaperones levels, PWS INS-1 {beta}-cells are more sensitive to ER stress, leading to earlier activation of all three arms of the unfolded protein response. These findings suggest that a chronic shortage of ER chaperones in PWS {beta}-cells leads to a deficiency of protein folding and/or delay in ER transit of insulin and other cargo. In summary, our results illuminate the pathophysiological basis of pancreatic {beta}-cell hormone deficits in PWS, with evolutionary implications for the multigenic PWS-domain, and indicate that PWS-imprinted genes coordinate concerted regulation of ER chaperone biosynthesis and {beta}-cell secretory pathway function.

genetics↗

bioRxiv2021

Proximity-based labeling reveals DNA damage-induced N-terminal phosphorylation of fused in sarcoma (FUS) leads to distinct changes in the FUS protein interactome.

Cytoplasmic accumulation of the RNA/DNA binding protein, fused in sarcoma (FUS), into inclusions is a common hallmark of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) pathology. We have previously shown that DNA damage can trigger the cytoplasmic accumulation of an N-terminally phosphorylated FUS. However, the functional consequences of N-terminal FUS phosphorylation are unknown. To gain insight into this question, we utilized proximity-dependent biotin labeling via ascorbate peroxidase 2 (APEX2) paired with mass-spectrometry (MS) to investigate whether N-terminal phosphorylation shifts the FUS protein-protein interaction network (interactome), and subsequently, its function. We report the first comparative analysis of the interactomes for three FUS variants: homeostatic wild-type FUS (FUS WT), a phosphomimetic variant of FUS (a proxy for N-terminally phosphorylated FUS, FUS PM), and a toxic FUS P525L mutant (a mutation that causes juvenile ALS, FUS P525L). Data are available via ProteomeXchange with identifier PXD026578. We demonstrate that compared to FUS WT and FUS P525L, the FUS PM interactome uniquely enriches for a set of cytoplasmic proteins that mediate mRNA metabolism and translation and nuclear proteins involved in spliceosome and DNA repair functions, respectively. We further identify and validate three proteins, VPS35, MOV10, and CLTA, as novel interacting partners of all three FUS variants. Lastly, we provide functional evidence that N-terminally phosphorylated FUS may disrupt homeostatic translation and steady state levels of specific mRNA transcripts. Taken together, these results highlight phosphorylation as a unique modulator of the FUS interactome and function.

neuroscience↗

bioRxiv2020

Biomarkers of lesion severity in a rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION)

The rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION) is similar in many of its pathophysiological responses to clinical NAION. However, little is known of the parameters associated with rNAION induction severity and if pre- or early post-induction biomarkers can be identified that enable prediction of lesion severity and ultimate loss of retinal ganglion cells (RGCs). Adult male Sprague-Dawley outbred rats were evaluated for various parameters including physiological characteristics (heart rate, respiratory rate, temperature, hematocrit), optic nerve head (ONH) appearance, pre- and post-induction mean diameter, and intravenous fluorescein and indocyanine green angiographic patterns of vascular leakage at 5 hours post-induction, performed using a spectral domain-optical coherence tomography (SD-OCT) instrument. These parameters were correlated with ultimate RGC loss by Brn3a (+) immunohistology. RGC loss also was correlated with the relative level of laser exposure. The severity of ONH edema 2d, but not 5hr, post induction was most closely associated with the degree of RGC loss, revealing a threshold effect, and consistent with a compartment syndrome where a minimum level of capillary compression within a tight space is responsible for damage. RGC loss increased dramatically as the degree of laser exposure increased. Neither physiological parameters nor the degree of capillary leakage 5hr post induction were informative as to the ultimate degree of RGC loss. Similar to human NAION, the rNAION model exhibits marked variability in lesion severity. Unlike clinical NAION, pre-induction ONH diameter likely does not contribute to ultimate lesion severity; however, cross-sectional ONH edema can be used as a biomarker 1-2d post-induction to determine randomization of subjects prior to inclusion in specific neuroprotection or neuroregeneration studies.

neuroscience↗

bioRxiv2020

Synergid calcium ion oscillations define a new feature of pollen tube reception critical for blocking interspecific hybridization

Reproductive isolation leads to the evolution of distinct new species, however, the molecular mechanisms that promote and maintain reproductive barriers are elusive. In flowering plants sperm cells are immotile and are delivered to female gametes by the pollen grain which germinates a polarized extension, the pollen tube, into floral tissue. After growing via polar extension to the female gametophyte, the pollen tube signals with receptive female cells flanking the egg in two distinct steps. If signaling is successful, the pollen tube releases sperm cells for fusion with female gametes. To better understand cell-cell recognition during reproduction, we investigated calcium ion dynamics associated with interspecific cell signaling between mating partners. We observed that interspecific pollen tubes successfully complete initial cell-cell signaling, but fail during later phases of pollen tube reception. Our work refines our understanding of pollen tube reception as a critical block to interspecific hybridization. Our results also shed light on the functional significance of the two phases of pollen tube reception, and implicate the second step as being the stage during which the pollen tube presents its genetic identity.

molecular biology↗

bioRxiv2019

Introduced species dominate different responses of grassland communities to climate change on serpentine and nonserpentine soils

Introduced species are a common feature of modern plant communities and experience environmental challenges alongside native species. Changes to the environment may reveal distinct species-environment relationships for native and introduced components of plant communities. Extreme environmental change, such as drought, is predicted to result in declines in native species and increased opportunities for invasion, but empirical support for these ideas remains mixed. We tested for differences in the response of native and invaded species to environmental changes by analyzing a longterm dataset of species abundance in California grasslands collected during a period of severe drought. Sampling sites included a combination of stressful serpentine soils, which are resilient against invasion and maintain diverse native species assemblages, and more benign nonserpentine soils, which are heavily invaded and harbor low levels of native species cover. We found a significant correlation between sampling year and species composition for nonserpentine sites, but not for serpentine sites. These patterns were repeated when only introduced species were included in the analysis but no pattern of change was found for native species. The species most strongly associated with directional change on nonserpentine soils were three invasive Eurasian grasses, Bromus hordaceus, Taeniatherium caput-medusae, and Avena fatua. Differences in species composition on both serpentine and nonserpentine soils were significantly correlated with specific leaf area, a trait which has been linked to drought tolerance in these communities, although changes in abundance for the three Eurasian grasses most strongly associated with change did not consistently follow this pattern. Our analyses indicate relatively stable native community composition and strong directional change in introduced species composition, contradicting predictions for how native and introduced species will respond to environmental shifts, but supporting the hypothesis that native and invading species groups have important functional differences that shape their relationships to the environment.

ecology↗

bioRxiv2019

Emergence of consciousness and complexity amidst diffuse delta rhythms: the paradox of Angelman syndrome

Numerous theories link consciousness to informationally rich, complex neural dynamics. This idea is challenged by the observation that children with Angelman syndrome (AS), while fully conscious, display a hypersynchronous electroencephalogram (EEG) phenotype typical of information-poor dynamics associated with unconsciousness. If informational complexity theories are correct, then sufficiently complex dynamics must still exist during wakefulness and exceed that observed in sleep despite pathological delta (1 - 4 Hz) rhythms in children with AS. As characterized by multiscale metrics, EEGs from 35 children with AS feature significantly greater complexity during wakefulness compared with sleep, even when comparing the most pathological segments of wakeful EEG to the segments of sleep EEG least likely to contain conscious experiences, and when factoring out delta power differences across states. These findings support theories linking consciousness with complexity and warn against reverse inferring an absence of consciousness solely on the basis of clinical readings of EEG.

neuroscience↗