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Abdullah, A.

Publications and source records attributed to Abdullah, A..

13 recordsLinked to original sources

Altered stimulus-specific adaptation at the auditory cortex of a mouse model of Fragile X Syndrome

Auditory hypersensitivity or decreased sound tolerance is a common phenotype of Fragile X Syndrome (FXS). Impairments in adaptation, defined as the reduction in the neuronal responsiveness to repeating sounds, can contribute to this prevalent phenotype. Previous studies on event-related potential observed impairments in mismatch negativity (MMN) in both FXS individuals and in the FMR1-knockout (KO) mouse model of FXS. Therefore, in the present study we characterized stimulus-specific adaptation (SSA), a neural correlate of MMN, at the auditory cortex (AC) of anesthetized (with ketamine/xylazine) female and male postnatal day 20 (P20) wild-type (WT) and FMR1-KO mice, using the oddball paradigm with either 4 Hz or 1 Hz repetition rate. We observed robust SSA at the 4 Hz repetition rate of the oddball paradigm in the AC neurons of all four groups of animals. We also noted that the strength of SSA diminished between 4 to 1 Hz repetition rate. In addition, at both the 4 Hz and 1 Hz repetition rate, reduced SSA was observed particularly in the male FMR1-KO mice compared to their WT counterparts, while female WT and FMR1-KO mice displayed similar SSA. In terms of sex differences, male FMR1-KO mice had lower SSA than female FMR1-KO mice, while SSA was similar in male and female WT mice. Overall, our observation of reduced SSA in the male FMR1-KO mice suggests that impairments in neuronal adaptation potentially contribute to the auditory hypersensitivity phenotype particularly within the male population.

neuroscience↗

Structural and functional basis of the non-canonical human Dicer-tRNA complex

Human Dicer (hDicer) is a key enzyme in the RNA interference (RNAi) pathway that generates [~]21-22 nt micro-RNA (miRNAs) and small interfering RNAs (siRNAs). We have previously shown that hDicer also generates tRNA-derived small RNAs (tsRNAs), which mediate nuclear gene silencing and regulate hundreds of disease-associated genes. As powerful and evolutionarily conserved cellular regulators, tsRNAs emerged as an important class of small RNAs. Therefore, it is essential to understand their biogenesis. However, the molecular and structural basis of tRNA cleavage by hDicer, as well as the role of chemical modifications such as 5-methylcytosine (m5C), in this process, remain unknown. Here, we present the first structural insights into hDicer in complex with tRNA, obtained by cryo-electron microscopy (cryo-EM), selective 2'-hydroxyl acylation analyzed by primer extension (SHAPE) and molecular dynamics (MD) simulations. Our results reveal that tRNAs adopt alternative conformations that are recognized and processed by hDicer. Furthermore, we show that tRNA cleavage by hDicer is facilitated by the m5C modification deposited by Nop2/SUN RNA methyltransferase 2 (NSUN2). Collectively, our findings redefine tRNAs as bona fide hDicer substrates and uncover a modification-dependent biogenetic pathway that reshapes the current understanding of the origins and regulation of human small RNAs. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=73 SRC="FIGDIR/small/744379v1_ufig1.gif" ALT="Figure 1000"> View larger version (24K): org.highwire.dtl.DTLVardef@14a8682org.highwire.dtl.DTLVardef@1c4d0daorg.highwire.dtl.DTLVardef@6bc433org.highwire.dtl.DTLVardef@11e27e1_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

Cross-Sectional Physiological and Neuromuscular Profiling of Elite and Recreational University Badminton Athletes: Preliminary Benchmarks for Exercise-Based Injury Risk Stratification

Background and PurposeBadminton imposes considerable cardiovascular and musculoskeletal stress. Physiological profiling can identify modifiable injury risk factors and inform exercise-based prevention and rehabilitation. This study compared cardiovascular recovery, neuromuscular activation, and limb strength between elite and recreational male university badminton players to derive preliminary physiological benchmarks for injury risk stratification and exercise rehabilitation guidance. MethodsForty male athletes (20 elite: national/university representatives with [&ge;]5 years of competitive experience; 20 recreational: <3 years of experience) completed assessments of heart rate recovery (HRR), biceps brachii surface electromyography (sEMG; SENIAM protocol), handgrip strength (JAMAR dynamometry), and maximal bodyweight squat repetitions. Independent-sample t-tests with Cohens d ( = 0.05) and Pearson correlations were applied. ResultsElite players demonstrated significantly greater handgrip strength (49.00{+/-}6.12 vs. 39.00{+/-}5.45 kg, p = 0.001, d = 1.72) and lower-limb (LL) strength (60.35{+/-}11.29 vs. 41.75{+/-}6.72 repetitions, p < 0.001, d = 1.96). Normalized sEMG root mean square (RMS) was higher in elite athletes during flexion (11.56{+/-}4.16% vs. 7.26{+/-}5.15%, p = 0.004, d = 0.94) and extension (12.67{+/-}4.56% vs. 7.85{+/-}5.73%, p = 0.003, d = 0.94). HRR did not differ significantly between groups (p = 0.17, d = 0.43, observed power = 0.34). Elite players nonetheless showed a more favorable recovery distribution. sEMG -HRR correlations were weak and non-significant in both groups. ConclusionsElite badminton players exhibit a distinct physiological profile of greater strength and more efficient neuromuscular activation. These preliminary cross-sectional findings may support the design of exercise-based injury-prevention and rehabilitation in university badminton.

biophysics↗

Early developmental characterization of gap-induced prepulse inhibition and habituation in the Fragile X Syndrome mouse model

IntroductionAtypical sensory processing, particularly auditory hypersensitivity, is a common and debilitating phenotype of Fragile X Syndrome (FXS). Electrophysiology studies in FMR1-knockout (KO) mice previously observed hyperexcitability at the auditory cortex (AC), with enhanced neuronal firing to auditory stimuli. Prepulse inhibition (PPI), a behavioral measure of sensorimotor gating, is robustly impaired in FXS individuals. Interestingly, a related paradigm called gap-induced inhibition of the acoustic startle (GPIAS) is mediated by the AC, and a previous study observed decreased GPIAS in mature FMR1-KO mice. Further, habituation is also an important sensory filtering mechanism, which has been reported to be impaired in mature FMR1-KO mice. However, not much is known about GPIAS and habituation in FMR1- KO mice during early development. MethodsWe evaluated GPIAS in male and female FMR1-KO mice at post-natal days 15 (P15), 20 (P20) and 30 (P30). The paradigm consisted of a prepulse stimulus (a gap in a continuous background noise) followed by a startle stimulus, with an inter-stimulus interval of 50 or 100 ms. Habituation was assessed prior to the GPIAS trials, with a series of startle only stimulus. ResultsWe observed a trend for genotype difference in acoustic startle response (ASR) magnitude, particularly in the female mice at P30. No significant genotype differences were noted in GPIAS or latency of ASR. Response duration was significantly increased in the male FMR1-KO mice compared to their WT counterparts during early development. Significant genotype differences were also observed in habituation and sensitization. In terms of development, we observed a significant increase in GPIAS with maturation. Furthermore, we also observed significant changes in the magnitude, response latency and duration of ASR with maturation. Finally, significant sex differences were observed in ASR magnitude and duration. ConclusionOur findings suggest that behavioral responses to auditory stimuli are dynamic during development and differ between females and males, an important consideration for future study design. Additionally, the FMR1-KO mice display habituation deficits during early development, which could be an ideal window for addressing auditory hypersensitivity in FXS.

neuroscience↗

Alterations in auditory midbrain processing is observed in both female andmale mouse model of Fragile X Syndrome

IntroductionSensory processing deficits presenting as auditory hypersensitivity is a common phenotype associated with Fragile X Syndrome (FXS), a leading monogenic cause of intellectual disability and autism spectrum disorder. Auditory hypersensitivity can also be observed in the FMR1-knockout (KO) mice, a well-established mouse model of autism and FXS. FXS is an X-linked disorder that is more prevalent in males compared to females, as a result most auditory and electrophysiology studies are performed in males. Previous in-vivo electrophysiology studies at the inferior colliculus (IC), an essential component of the auditory pathway, in male FMR1-KO mice at post-natal days 14, 21 and 34 (P14, P21 and P34) demonstrated increased neuronal firing, suggesting that the IC could play a role in auditory hypersensitivity. However, very little is known about the role of the central nucleus of the IC (ICc) and auditory hypersensitivity in females. MethodsHere we investigated auditory processing at P20 and P30, representative of early and late developmental stage of auditory development, respectively, at the central nucleus of the IC (ICc) of both female and male FMR1-KO mice, compared with wildtype (WT) animals. ResultsIn-vivo electrophysiology recordings from the ICc neurons of the FMR1-KO mice at both developmental ages demonstrated increased response magnitude measured by spike number to pure tones of varying frequency and amplitude, compared with age- and sex-matched WT animals. In addition, within the FMR1-KO group we also observed significant developmental and sex difference wherein higher response magnitudes were displayed at P20 and in the female mice. Minimum threshold of ICc neuron in the KO mice was significantly decreased at both P20 and P30. The ICc neurons in the KO mice also displayed increased response duration compared to WT animals at both P20 and P30, but significant sex difference was only observed at P30. Our data also indicated that the ICc neurons of both groups displayed weak negative relationship between latency and response magnitude at P20, and at P30 the WT mice showed a stronger relationship only in the female group. In terms of developmental changes, we observed decreasing neuronal firing only in the KO mice between 20- and 30-day old female and male mice. Reduced response duration was observed in 30-day old mice of both sexes of both genotypes. Regarding minimum threshold, we observed a decline between early and late auditory development only in the male mice. Finally, our results also indicated that in the WT mice the reverse relationship between latency and response magnitude became more pronounced and consistent with age, a developmental trend that was absent in both the female and male FMR1-KO mice. DiscussionOverall, our findings demonstrate that auditory processing deficits can also be observed in the female FMR1-KO mice using in-vivo electrophysiology studies, highlighting the importance of including female subjects in future studies. These results also indicate that auditory hypersensitivity can be observed robustly in younger mice, suggesting that the early development stage could be an ideal target for interventions.

neuroscience↗

A unifying model of species abundance distribution

The species abundance distribution (SAD) is one of the most fundamental and best-studied macroecological patterns at the core of any biodiversity theory. Remarkably, almost every community investigated to date shows a hollow curve, indicative of the presence of many rare species and a few abundant species. While the precise nature of SAD is believed to reflect fundamental ecological processes underlying community assembly, ecologists have yet to identify a single model that comprehensively explains all SADs. Recent studies using large datasets suggested that logseries best describes animal and plant communities1,2 while lognormal is the best model for microbes3, thereby challenging the notion of a unifying SAD model across the tree of life. Using a large dataset of [~]30,000 globally distributed communities spanning animals, plants and microbes from diverse environments, here we show that powerbend distribution, predicted by a maximum information entropy-based theory of ecology, emerges as a unifying model that accurately captures SADs of all life forms, habitats and abundance scales, supporting the existence of universal ecological principles. Our findings reject the notion of pure neutrality and support the idea that community assembly is driven by both random fluctuations and deterministic mechanisms, such as interspecific trait variation and resource competition. We also show that the previously estimated one trillion microbial species existing on Earth might be orders of magnitude off.

ecology↗

Exploring the Dynamics of Social Interactions During the Juvenile Stage in a Mouse Model of Fragile X Syndrome

IntroductionFragile X Syndrome (FXS), caused by Fmr1 mutations, is linked to cognitive and behavioral differences, including altered social interactions. Most mouse studies focus on adults, despite human research showing critical developmental changes in childhood and adolescence. We examined social behavior in juvenile male and female Fmr1 knockout (KO) mice as well as heterozygous (HET) females. We further assessed cortical activity in KO females to better understand early phenotypes. MethodsJuvenile mice of both sexes and genotypes were paired in same-sex, novel dyads for 10-minute interactions. Key social behaviors such as head, anogenital, and body sniffing, and physical touch, as well as distance travelled, were analyzed with a marker-less tracking software. Frontal-parietal EEG recordings were collected from wild-type (WT) and KO females in home cage and social contexts to analyze power spectra across frequency bands. ResultsHET and KO females engaged in more frequent but shorter interaction events compared to WT females, with HET females showing the highest counts. Males displayed similar trends when comparing KO and WT. Males engaged in overall higher interaction events than females. EEG analyses revealed altered oscillatory activity in KO females compared to WT females, especially within theta, alpha, and beta bands, most prominently during the early interaction phase. Locomotor activity correlated weakly with head/anogenital sniffing but more strongly with body sniffing and touch. DiscussionThese findings suggest that Fmr1-related differences in juvenile social behavior are sex-dependent and associated with cortical oscillatory changes. Characterizing these early phenotypes in both sexes allows us to further understand FXS development and informs potential routes for early intervention. Key PointsO_LIFragile X Syndrome (FXS), the leading inherited cause of autism, is associated with disruptions in social behavior. C_LIO_LIWhile social phenotypes are relatively well described in adult mouse models of FXS, juvenile manifestations remain poorly understood. C_LIO_LISocial behavior was assessed in juvenile male and female Fmr1 knockout (KO), heterozygous (HET, female only), and wildtype (WT) mice, and frontal-parietal EEG recordings were collected from WT and KO females. C_LIO_LIHET and KO females exhibited more frequent but shorter social interactions than WT females, with HET showing the greatest number of events. Males showed similar patterns when comparing KO and WT. Males engaged in higher overall interaction events than females. EEG recordings revealed altered oscillatory activity in KO compared to WT females, most pronounced during the early phase of social encounter. C_LIO_LIThese findings reveal sex- and genotype-dependent differences in juvenile social behavior and cortical activity, highlighting the importance of studying juvenile development in FXS. C_LI

animal behavior and cognition↗

Global brain health modulates the impact of lesion damage on post-stroke sensorimotor outcomes

Sensorimotor performance after stroke is strongly related to focal injury measures such as corticospinal tract lesion load. However, the role of global brain health is less clear. Here, we examined the impact of brain age, a measure of neurobiological aging derived from whole brain structural neuroimaging, on sensorimotor outcomes. We hypothesized that stroke lesion damage would result in older brain age, which would in turn be associated with poorer sensorimotor outcomes. We also expected that brain age would mediate the impact of lesion damage on sensorimotor outcomes and that these relationships would be driven by post-stroke secondary atrophy (e.g., strongest in the ipsilesional hemisphere in chronic stroke). We further hypothesized that structural brain resilience, which we define in the context of stroke as the brains ability to maintain its global integrity despite focal lesion damage, would differentiate people with better versus worse outcomes. We analyzed cross-sectional high-resolution brain MRI and outcomes data from 963 people with stroke from 38 cohorts worldwide using robust linear mixed-effects regressions to examine the relationship between sensorimotor behavior, lesion damage, and brain age. We used a mediation analysis to examine whether brain age mediates the impact of lesion damage on stroke outcomes and if associations are driven by ipsilesional measures in chronic ([&ge;]180 days) stroke. We assessed the impact of brain resilience on sensorimotor outcome using logistic regression with propensity score matching on lesion damage. Stroke lesion damage was associated with older brain age, which in turn was associated with poorer sensorimotor outcomes. Brain age mediated the impact of corticospinal tract lesion load on sensorimotor outcomes most strongly in the ipsilesional hemisphere in chronic stroke. Greater brain resilience, as indexed by younger brain age, explained why people have better versus worse sensorimotor outcomes when lesion damage was fixed. We present novel evidence that global brain health is associated with superior post-stroke sensorimotor outcomes and modifies the impact of focal damage. This relationship appears to be due to post-stroke secondary degeneration. Brain resilience provides insight into why some people have better outcomes after stroke, despite similar amounts of focal injury. Inclusion of imaging-based assessments of global brain health may improve prediction of post-stroke sensorimotor outcomes compared to focal injury measures alone. This investigation is important because it introduces the potential to apply novel therapeutic interventions to prevent or slow brain aging from other fields (e.g., Alzheimers disease) to stroke.

neuroscience↗

In vivo emergence of high-level resistance during treatment reveals the first identified mechanism of amphotericin B resistance in Candida auris

Candida auris has emerged as a healthcare-associated and multidrug-resistant fungal pathogen of great clinical concern. While as much as 50% of C. auris clinical isolates are reported to be resistant to amphotericin B, to date, no mechanisms contributing to this resistance have been identified. We report here mutations in the C. auris sterol-methyltransferase gene, ERG6, as the first identified mechanism of amphotericin B resistance in this emerging pathogen and describe the clinical case in which this high-level amphotericin B resistance was acquired in vivo during therapy. Whole genome sequencing revealed the four C. auris isolates obtained from this single patient case to be genetically related and identified a mutation in ERG6 as being associated with amphotericin B resistance. Cas9-mediated genetic manipulations confirmed this mutation alone to confer a >32-fold increase in amphotericin B resistance, and comprehensive sterol profiling revealed an abrogation of ergosterol biosynthesis and a corresponding accumulation of cholesta-type sterols in isolates and strains harboring the clinically derived ERG6 mutation. Together these findings represent the first significant step forward in the understanding of clinical amphotericin B resistance in C. auris.

microbiology↗

Plastid genomics of Nicotiana (Solanaceae): insights into molecular evolution, positive selection and the origin of the maternal genome of Aztec tobacco (Nicotiana rustica)

The genus Nicotiana of the family Solanaceae, commonly referred to as tobacco plants, are a group cultivated as garden ornamentals. Besides their use in the worldwide production of tobacco leaves, they are also used as evolutionary model systems due to their complex development history, which is tangled by polyploidy and hybridization. Here, we assembled the plastid genomes of five tobacco species, namely N. knightiana, N. rustica, N. paniculata, N. obtusifolia and N. glauca. De novo assembled tobacco plastid genomes showed typical quadripartite structure, consisting of a pair of inverted repeats (IR) regions (25,323-25,369 bp each) separated by a large single copy (LSC) region (86,510 -86,716 bp) and a small single copy (SSC) region (18,441-18,555 bp). Comparative analyses of Nicotiana plastid genomes showed similar GC content, gene content, codon usage, simple sequence repeats, oligonucleotide repeats, RNA editing sites and substitutions with currently available Solanaceae genomes sequences. We identified twenty highly polymorphic regions mostly belonging to intergenic spacer regions (IGS), which could be appropriate for the development of robust and cost-effective markers to infer the phylogeny of genus Nicotiana and family Solanaceae. Our comparative plastid genome analysis revealed that the maternal parent of the tetraploid N. rustica was the common ancestor of N. paniculata and N. knightiana, and the later species is more closely related to N. rustica. The relaxed molecular clock analyses estimated that the speciation event between N. rustica and knightiana appeared 0.56 Ma (HPD 0.65-0.46). The biogeographical analysis showed a south-to-north range expansion and diversification for N. rustica and related species, where N. undulata and N. paniculata evolved in North/Central Peru, while N. rustica developed in Southern Peru and separated from N. knightiana, which adapted to the Southern coastal climatic regimes. We further inspected selective pressure on protein-coding genes among tobacco species to determine if this adaptation process affected the evolution of plastid genes. These analyses indicated that four genes involved in different plastid functions, such as DNA replication (rpoA) and photosynthesis (atpB, ndhD and ndhF), came under positive selective pressure as a result of specific environmental conditions. Genetic mutations of the following genes might have contributed to the survival and better adaptation during the evolutionary history of tobacco species.

genomics↗

Regulation of nerve growth and patterning by cell surface protein disulphide isomerase

Contact repulsion of growing axons is an essential mechanism for spinal nerve patterning. In birds and mammals the embryonic somites generate a linear series of impenetrable barriers, forcing axon growth cones to traverse one half of each somite as they extend towards their body targets. This study shows that protein disulphide isomerase provides a key component of these barriers, mediating contact repulsion at the cell surface in half-somites. Repulsion is reduced both in vivo and in vitro by a range of methods that inhibit enzyme activity. The activity is critical in initiating a nitric oxide/S-nitrosylation-dependent signal transduction pathway that regulates the growth cone cytoskeleton. Rat forebrain grey matter extracts contain a similar activity, and the enzyme is expressed at the surface of cultured human astrocytic cells and rat cortical astrocytes. We suggest this system is co-opted in the brain to counteract and regulate aberrant nerve terminal growth.

developmental biology↗

IRE1α is critical for kaempferol induced neuroblastoma differentiation

Neuroblastoma is an embryonic malignancy arises out of the neural crest cells of the sympathetic nervous system. It is the most common childhood tumor and well known for its spontaneous regression via the process of differentiation. The induction of differentiation using small molecule modulators such as all trans retinoic acid is one of the treatment strategies to treat the residual disease. In this study, we have reported the effect of kaempferol, a phytoestrogen in inducing differentiation of neuroblastoma cells in vitro. Treatment of neuroblastoma cells with kaempferol reduced the proliferation and enhanced apoptosis along with the induction of neuritogenesis. Analysis of the expression of neuron specific markers such as {beta} III tubulin, neuron specific enolase and NRDG1 (N-myc down regulated gene 1) revealed the process of differentiation accompanying kaempferol induced apoptosis. Further analysis on understanding the molecular mechanism of action showed that the activity of kaempferol happened through the activation of the endoribonuclease activity of IRE1 (Inositol requiring enzyme 1 alpha), an endoplasmic reticulum (ER) resident transmembrane protein. The in silico docking analysis and biochemical assays using recombinant human IRE1 confirms the binding of kaempferol to the ATP binding site of IRE1 and thereby activating ribonuclease activity. Treatment of cells with the small molecule inhibitor STF083010 which specifically targets and inhibits the endoribonuclease activity of IRE1 showed reduced expression of neuron specific markers and curtailed neuritogenesis. The knock down of IRE1 using plasmid based shRNA lentiviral particles also showed diminished changes in the change in morphology of the cells upon kaempferol treatment. Thus our study suggests that kaempferol induces differentiation of neuroblastoma cells via the IRE1-XBP1 pathway.

molecular biology↗

Identification of FDA-approved drugs as novel allosteric inhibitors of human executioner caspases

The regulation of apoptosis is a tightly-coordinated process and caspases are its chief regulators. Of special importance are the executioner caspases, caspase-3/7, the activation of which irreversibly sets the cell on the path of death. Dysregulation of apoptosis, particularly an increased rate of cell death lies at the root of numerous human diseases. Although several peptide-based inhibitors targeting the homologous active site region of caspases have been developed, owing to their non-specific activity and poor pharmacological properties their use has largely been restricted. Thus, we sought to identify FDA-approved drugs that could be repurposed as novel allosteric inhibitors of caspase-3/7. In this study, we virtually screened a catalog of FDA-approved drugs targeting an allosteric pocket located at the dimerization interface of caspase-3/7. From among the top-scoring hits we short-listed five compounds for experimental validation. Our enzymatic assays using recombinant caspase-3 suggested that four out of the five drugs effectively inhibited caspase-3 enzymatic activity in vitro with IC50 values ranging ~10-55 M. Structural analysis of the docking poses show the four compounds forming specific non-covalent interactions at the allosteric pocket suggesting that these molecules could disrupt the adjacently-located active site. In summary, we report the identification of four novel non-peptide allosteric inhibitors of caspase-3/7 from among FDA-approved drugs.

bioinformatics↗