bioRxiv Science⌕ Search

Biology subjects

Poljak, A.

Publications and source records attributed to Poljak, A..

8 recordsLinked to original sources

Synaptic proteomics identifies cathepsin B as a regulator of synapse remodelling during learning

Learning requires dynamic changes in synaptic protein composition. Most synaptic proteomic studies capture endpoint snapshots following training, overlooking molecular changes occurring during learning itself. We previously established TurboID proximity proteomics as an approach to capture protein-level changes during learning in the nervous system of Caenorhabditis elegans. Here, we apply this strategy to synapses. Trained synapses exhibited a distinct proteome compared with mock-trained controls, with pathways enriched for neurotransmission, synaptic reorganisation, protein trafficking, and autophagy. Enrichment of autophagy proteins led us to investigate the cathepsin B orthologue CPR-4, a previously uncharacterised candidate for learning identified exclusively in trained synapses. Functional validation identified CPR-4 as a novel regulator of memory: CPR-4 is required for learning, and the absence of CPR-4 results in trained synaptic proteomes that are more like those of mock-trained synapses. Our findings support a model through which CPR-4 promotes synaptic remodelling required for learning through targeted protein clearance.

neuroscience↗

The long noncoding RNA Dory is required for female but not male spatial learning and memory

Large numbers of long noncoding RNAs (lncRNAs) exhibit region- or cell-specific expression and subcellular locations in the mammalian brain. We analyzed the expression and function of the mouse lncRNA 2700046G09Rik (also called Sgms1os1), which we have named Dory due to sex-specific disruption of spatial memory in rodent gene knockout and RNA knockdown. We show that Dory is predominantly expressed in a punctate pattern in nuclei of excitatory neurons in the hippocampus, and in both neuronal and non-neuronal cells in the cerebellum. We show by high resolution RNA sequencing that Dory brain transcripts are composed of 1-3 exons with multiple isoforms. Deletion of the constitutive first exon of Dory by CRISPR-Cas9 genome editing resulted in the impairment of spatial memory and some aspects of balance in female but not male mice. Dory-null mice presented without overt changes in brain morphology. Knockdown of the rat homolog of Dory in dorsal hippocampus using antisense oligonucleotides confirmed inhibition of spatial memory in females only. RNA sequencing and mass spectrometry revealed differential hippocampal gene and protein expression profiles, notably of prolactin, growth hormone and pro-opiomelanocortin, between male and female Dory knockout mice.

neuroscience↗

A proteomic signature of oocyte quality from models of varying oocyte developmental competence

Study questionWhich proteins underpin oocyte developmental competence, as modelled by oocytes of variable competence matured in vivo, or matured in vitro under different conditions (capacitation in vitro maturation (CAPA) or standard in vitro maturation (IVM))? Summary answerSignificant differences in the global proteome were observed in both oocytes and their corresponding cumulus cells depending on the mode of oocyte maturation, with key variations in eukaryotic translation, autophagy and endocytosis pathways within oocytes, and changes in reactive oxygen species detoxification and serine biosynthesis in cumulus cells. What is known alreadyWithin the ovarian follicle, mammalian oocytes must acquire the necessary molecular machinery to support successful fertilisation and embryonic development. Close contact with the surrounding cumulus cells ensures coordinated nuclear and cytoplasmic maturation of the oocyte, along with the accumulation of proteins stored within the oocyte in cytoplasmic lattices and endo-lysosomal vesicular assemblies. Study design, size, durationThis basic science study utilised a mouse model to assess proteomic changes across three oocyte competence models. Key proteins identified in mouse oocytes were also assessed in discarded immature human germinal vesicle (GV) oocytes and MII oocytes following rescue-IVM. Three oocyte maturation methods were tested: i) in vivo maturation, (ii) CAPA and (iii) standard IVM. In vivo maturation served as a positive control group, whereby metaphase II (MII) mature oocytes were collected from mice stimulated with pregnant mare serum gonadotropin (PMSG) and triggered with human chorionic gonadotropin (hCG), simulating full ovarian stimulation. For the in vitro maturation groups, immature cumulus oocyte complexes (COCs) were collected from mildly stimulated (23 hr PMSG) mice. For the standard IVM group, immature COCs were matured in media containing amphiregulin and epiregulin for 18 hours. For the CAPA group, COCs were held for 24 hours in pre-IVM conditions in the presence of c-type natriuretic peptide (CNP), oestradiol, insulin and follicle stimulating hormone (FSH), and then matured via IVM in media containing FSH, amphiregulin and epiregulin. Four biological replicates were performed for mouse proteomics experiments, three biological replicates performed for mouse immunocytochemistry experiments and six replicates were performed for embryology experiments. Participants/materials, settings, methodsFour to six-week-old C57BL/6JAusb mice were used for all mouse experiments. Embryology outcomes were used to confirm the variation in oocyte developmental competence between the three maturation groups. For the in vivo, CAPA and IVM groups, mature MII COCs were collected and separated into oocytes and cumulus cells. Oocytes and cumulus cells were subjected to mass spectrometry and bioinformatic analysis was performed using Proteome Discoverer and Ingenuity Pathway Analysis, with data validated by immunofluorescence. To assess conservation of proteins in human oocytes, 49 oocytes were collected from 36 patients following assisted reproduction technology (ART) cycles and subject to immunofluorescence. Rescue-IVM was also performed with half of the human oocyte cohort to obtain MII oocytes. Main results and the role of chanceProteomic profiling identified around 1600 proteins in mouse oocytes and 3100 in mouse cumulus cells across all three treatment groups (at least 2 peptides per protein). Differential expression analysis and pattern analysis collectively revealed a signature of proteins that were consistently differentially expressed between in vivo and in vitro oocyte maturation systems (log2FC of {+/-} 1 and a p-value [≤] 0.05). These subsets of proteins were mapped to biological processes including eukaryotic translation, autophagy and endocytosis pathways within oocytes. Orthogonal validation of clathrin, ribosomal protein L24 and eukaryotic initiation factor 2A supported the proteomic findings and expression was conserved in human oocytes. Changes in reactive oxygen species detoxification and serine biosynthesis were observed in mouse cumulus cells, with fluorescence intensity changes in ferredoxin-1 and phosphoglycerate dehydrogenase supporting the dysregulation of cumulus cell processes during in vitro maturation. Large scale dataThe mass spectrometry data are available via ProteomeXchange with identifier PXD073269. Limitations, reasons for cautionThe foundational mechanisms of oocyte developmental competence remain elusive, particularly in humans where MII oocytes are heterogenous in quality within the same stimulation cycle and patient. In this study, C57Bl6/J mice were used as the model species, allowing precise control over differing models of oocyte quality and capacity to analyse large numbers of oocytes. However, care is required when interpreting the significance of these findings in mice to mechanisms regulating human oocyte quality. Nonetheless, the in vivo stimulation and both IVM protocols used in this study are clinically relevant and developmentally matched. This study has also not addressed oocyte developmental competence in gonadotropin-free IVM oocytes, which is now a clinical reality. Wider implications of the findingsThis study confirms that mouse oocytes, matured in vitro in two clinically relevant systems, show reduced developmental competence when compared to in vivo matured oocytes. Through examination of the global proteome in oocytes, molecular pathways including eukaryotic translation, autophagy and endocytosis were dysregulated in in vitro oocytes. Recent findings have revealed the critical role of these pathways to developmental competence in the context of in vivo development. In cumulus cells, changes in reactive oxygen species detoxification and serine biosynthesis were observed, adding to the extensive knowledge around metabolic activity in cumulus cells as a critical facet of oocyte quality. Combined, this data suggests that the necessary processes of protein storage and degradation in oocytes and metabolism in cumulus cells constitute important components of oocyte quality. These processes appear suboptimal in current IVM systems, providing a future research direction to optimise IVM protocols with consideration to these protein pathways. Study funding/competing interestsThis study was funded by a National Health and Medical Research Council Investigator Fellowship (APP1023210) awarded to R.B.G. and by a gift from Open Philanthropy. The following competing interests are declared: R.B.G.is a consultant to Dioseve Inc.. L.E.W is a co-founder, shareholder, director and advisor of Jumpstart Fertility Inc.. L.E.W. is also an advisor and shareholder in EdenRoc Sciences, the parent company of Metro Biotech NSW and Metro Biotech, and in Life Biosciences LLC and its daughter companies. His UNSW Industry Scientia position is partly funded by Proto Axiom. All other authors have no competing interests to disclose.

cell biology↗

Identifying regulators of associative learning using a protein-labelling approach in C. elegans

The ability to learn and form memories is critical for animals to make choices that promote their survival. The biological processes underlying learning and memory are mediated by a variety of genes in the nervous system, acting at specific times during memory encoding, consolidation, and retrieval. Many studies have utilised candidate gene approaches or random mutagenesis screens in model animals to explore the key molecular drivers for learning and memory. We propose a complementary approach to identify this network of learning regulators: the proximity-labelling tool TurboID, which promiscuously biotinylates neighbouring proteins, to snapshot the proteomic profile of neurons during learning. To do this, we expressed the TurboID enzyme in the entire nervous system of C. elegans and exposed animals to biotin only during the training step of an appetitive gustatory learning paradigm. Our approach revealed hundreds of proteins specific to trained worms, including components of molecular pathways previously implicated in memory in multiple species such as insulin signalling, G protein-coupled receptor signalling, and MAP kinase signalling. Most (87-95%) of the proteins identified are neuronal, with relatively high representation for neuron classes involved in locomotion and learning. We validated several novel regulators of learning, including cholinergic receptors (ACC-1, ACC-3, LGC-46) and putative arginine kinase F46H5.3. These previously uncharacterised learning regulators all showed a clear impact on appetitive gustatory learning, with F46H5.3 showing an additional effect on aversive gustatory memory. Overall, we show that proximity labelling can be used in the brain of a small animal as a feasible and effective method to advance our knowledge on the biology of learning.

neuroscience↗

Oocyte and cumulus cell cooperativity and metabolic plasticity under the direction of oocyte paracrine factors

Mammalian oocytes develop and mature in a mutually dependent relationship with surrounding cumulus cells. The oocyte actively regulates cumulus cell differentiation and function by secreting soluble paracrine oocyte-secreted factors (OSFs). We characterized the molecular mechanisms by which two model OSFs, cumulin and BMP15, regulate oocyte maturation and cumulus-oocyte cooperativity. Exposure to these OSFs during maturation altered the proteomic and multispectral autofluorescence profiles of both the oocyte and cumulus cells. In oocytes, cumulin significantly upregulated proteins involved in nuclear function. In cumulus cells, both OSFs elicited marked upregulation of a variety of metabolic processes (mostly anabolic), including lipid, nucleotide, and carbohydrate metabolism, while mitochondrial metabolic processes were downregulated. The mitochondrial changes were validated by functional assays confirming altered mitochondrial morphology, respiration, and content, whilst maintaining ATP homeostasis. Collectively, these data demonstrate that OSFs remodel cumulus cell metabolism during oocyte maturation in preparation for ensuing fertilization and embryonic development. HIGHLIGHTSO_LIDuring oocyte maturation, oocyte-secreted factors promote cell cooperativity between the oocyte and cumulus cells by altering the molecular composition of both cell types. C_LIO_LIOocyte-secreted factors downregulate protein catabolic processes, and upregulate DNA binding, translation, and ribosome assembly in oocytes. C_LIO_LIOocyte-secreted factors alter mitochondrial number, morphology, and function in cumulus cells. C_LIO_LIOocyte-secreted factors further enhance metabolic plasticity in cumulus cells by upregulating anabolic pathways for macromolecules and small molecule organics. C_LIO_LIThe oocyte, via oocyte-secreted factors, instructs cumulus cells to increase metabolic workload on its behalf, thereby subduing oocyte metabolism. C_LI

developmental biology↗

Deep proteome analysis of plasma reveals novel biomarkers of mild cognitive impairment and Alzheimer's disease: A longitudinal study

Ageing is the primary risk factor for AD; however, there is a poor understanding of the biological mechanisms by which the ageing process contributes to the development of AD in some individuals, while others progress to advanced age with relatively little AD neuropathology. To halt the progression of AD, the preclinical stage of neurodegeneration (before the onset of clinical symptoms) is anticipated to be the more effective time point for applying potentially disease-modifying interventions in AD. The main objective of this study was to understand the age and disease related proteomic changes are detectable in plasma, based on retrospective analysis of longitudinal data and cross-sectional analyses of clinically diagnosed cases. We conducted an in-depth plasma proteomics analysis using intensive depletion of high-abundant plasma proteins using the Agilent multiple affinity removal liquid chromatography (LC) column-Human 14 (Hu14) followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS PAGE) technique. In this study, we have begun to address the following questions; (1) differences in plasma proteomic profiles between normal ageing, vs ageing with progress to cognitive decline (MCI) or disease (dementia, probable AD), (2) cross-sectional analysis of baseline data, when all subjects are clinically identified as cognitively normal, provides insight into the preclinical changes which precede subsequent progression to AD and potentially provide early biomarkers, and (3) comparison of plasma at the point of progression to clinically diagnosed onset of cognitive decline or AD, can provide potential plasma biomarkers to facilitate clinical diagnosis. Furthermore, our findings also identified some proteins previously discovered in AD CSF and brain proteomics signatures that could provide clinically meaningful information. We identified differentially expressed proteins which were associated with several biological and molecular processes that may serve as therapeutic targets and fluid biomarkers for the disease.

neuroscience↗

Impact of APOE e3 and e4 genotypes on plasma proteome signatures in Alzheimer's disease

The {varepsilon}4 allele of the apolipoprotein E (APOE) gene is a high-risk factor for Alzheimers disease (AD). However, approximately 25%-40% of patients with AD do not carry the APOE{varepsilon}4 allele, and the pathophysiological mechanisms underlying AD are less evident in these individuals. The main objective of this study was to understand better the changes in plasma that may contribute to disease pathogenesis in AD and how APOE{varepsilon}3 and APOE{varepsilon}4 contribute to biomarker profiles in AD. We conducted an in-depth plasma proteomics analysis using intensive depletion of high-abundant plasma proteins using the Agilent multiple affinity removal liquid chromatography (LC) column-Human 14 (Hu14) followed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS PAGE) technique. In this study, we identified a high number of protein expression alterations in plasma which were found uniquely in APOE{varepsilon}3 and APOE{varepsilon}4 carriers. These differentially expressed proteins (DEPs) were associated with several molecular functions, including complement cascade, glycolysis, metabolism, plasma lipoprotein assembly, remodelling, and clearance. In addition to unique changes in both APOE genotypes, many proteins were also dysregulated in the presence of both APOE{varepsilon}3 and APOE{varepsilon}4 genotypes depicting the involvement of these proteins in the pathogenesis of AD regardless of the APOE genotypes. We also compared the plasma proteomes of{varepsilon} 4 and{varepsilon} 3 carriers in normal controls, which provided insight into factors that may provide protection from progression to AD despite the presence of the{varepsilon} 4 allele. Furthermore, our findings also identified some proteins previously discovered in AD CSF and brain proteomics signatures that could provide clinically meaningful information.

neuroscience↗

Genetic and environmental determinants of variation in the plasma lipidome of older Australian twins

The critical role of blood lipids in a broad range of health and disease states is well recognised, while an understanding of the complex genetic regulation of lipid homeostasis is emerging. Traditional blood lipids (LDL-C, HDL-C and triglycerides) are known to be substantially regulated by genetic variation. Less well explored is the interplay of genetics and environment within the broader blood lipidome. Here we use the twin model to examine heritability of the plasma lipidome among healthy older aged twins and explore gene expression and epigenetic (DNA methylation) associations of these lipids. Heritability of 209 plasma lipids quantified by liquid chromatography coupled mass spectrometry (LC-MS) was assessed in 75 monozygotic and 55 dizygotic twin pairs enrolled in the Older Australian Twins Study (OATS), aged 69-93 years. Only 27/209 lipids (13.3%) were significantly heritable under the classical ACE twin model (h2 = 0.28-0.59). Ceramides (Cer) and triglycerides (TG) were most heritable, while sphingomyelins (SM) and most phospholipids, especially lysophospholipids, were not significantly heritable. Lipid levels correlated with 3731 transcripts. Relative to non-significantly heritable TGs, heritable TGs had a greater number of associations with gene transcripts, which were not directly associated with lipid metabolism, but with immune function, signalling and transcriptional regulation. Genome-wide average DNA methylation (GWAM) levels accounted for a proportion of variability in some non-heritable lipids, especially lysophosphatidylcholine (LPC). We found a complex interplay of genetic and environmental influences on the ageing plasma lipidome, with most of the variation controlled by unique environmental influences.

genetics↗