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bioRxiv2025

The break in the cycle: Inositol pyrophosphate fluxomics disentangled via mathematical modelling

This study investigates the metabolic pathways of inositol pyrophosphates (IPPs) in the yeast cell line {Delta}SPX and the human tumor cell line HCT116. Utilizing pulse-labelling experiments with 18O water and ordinary differential equation (ODE) models, we explore the synthesis and turnover of the highly phosphorylated IPP, 1,5-InsP8. Our findings challenge the notion that 1,5-InsP8 can be synthesized through distinct routes, revealing a linear reaction sequence in both systems. Employing model reduction via the profile likelihood method, we achieved statistically concise identifiability analysis that led to significant biological insights. In yeast, we determined that 1,5-InsP8 production primarily occurs through the phosphorylation of 5-InsP7, with the pathway involving 1-InsP7 deemed unnecessary as its removal did not compromise model accuracy. In HCT116 cells, 1,5-InsP8 synthesis is mainly driven by 1-InsP7, with variations observed across different experimental conditions. These results underscore the utility of model reduction in enhancing our understanding of metabolic pathways, challenging traditional views of IPP metabolism, and providing a framework for future investigations into the regulation and implications of linear IPP pathways in eukaryotic cells.

molecular biology↗

bioRxiv2022

Metabolic-imaging of human glioblastoma explants: a new precision-medicine model to predict tumor treatment response early

BackgroundGlioblastoma (GB) is the most severe form of brain cancer, with a 12-15 month median survival. Surgical resection, temozolomide (TMZ) treatment, and radiotherapy (RT) remain the primary therapeutic options for GB, and no new therapies have been introduced in recent years. This therapeutic standstill is primarily due to preclinical approaches that do not fully respect the complexity of GB cell biology and fail to test efficiently anti-cancer treatments. Therefore, better treatment screening approaches are needed. In this study, we have developed a novel functional precision medicine approach to test the response to anticancer treatments in organoids derived from the resected tumors of glioblastoma patients. MethodsGB organoids were grown for a short period of time to prevent any genetic and morphological evolution and divergence from the tumor of origin. We chose metabolic imaging by NAD(P)H fluorescence lifetime imaging microscopy (FLIM) to predict early and non-invasively ex-vivo anti-cancer treatment responses of GB organoids. TMZ was used as the benchmark drug to validate the approach. Whole-transcriptome and whole-exome analyses were then performed to characterize tumor cases stratification. ResultsOur functional precision medicine approach was completed within one week after surgery and two groups of TMZ Responder and Non Responder tumors were identified. FLIM-based metabolic tumor stratification was well-reflected at the molecular level, confirming the validity of our approach, highlighting also new target genes associated with TMZ treatment and identifying a new 17 gene molecular signature associated with survival. The number of promoter methylated tumors for the MGMT gene was higher in the responsive group, as expected, however, some non-methylated tumor cases turned out to be nevertheless responsive to TMZ, suggesting that our procedure could be synergistic with the classical MGMT methylation biomarker. ConclusionsFor the first time, FLIM-based metabolic imaging was used on ex-vivo live glioblastoma organoids. Unlike other approaches, ex-vivo patient-tailored drug response is performed at an early stage of tumor culturing with no animal involvement and with minimal tampering with the original tumor cytoarchitecture. This functional precision medicine approach can be exploited in a range of clinical and laboratory settings to improve the clinical management of GB patients and implemented on other cancers as well.

molecular biology↗

bioRxiv2021

Diversification of Transcription Factor NF-κB in Protists

In this report, we investigate the evolution of transcription factor NF-{kappa}B by examining its structure, activity, and regulation in two protists using phylogenetic, cellular, and biochemical techniques. In Capsaspora owczarzaki (Co), we find that full-length NF-{kappa}B has an N-terminal DNA-binding domain and a C-terminal Ankyrin (ANK) repeat inhibitory domain, and its DNA-binding activity is more similar to metazoan NF-{kappa}B rather than Rel proteins. As with mammalian NF-{kappa}B proteins, removal of the ANK repeats is required for Co-NF-{kappa}B to enter the nucleus, bind DNA, and activate transcription. However, C-terminal processing of Co-NF-{kappa}B is not induced by co-expression of IKK in human cells. Exogenously expressed Co-NF-{kappa}B localizes to the nucleus in Co cells. NF-{kappa}B mRNA and DNA-binding levels differ across three life stages of Capsaspora, suggesting distinct roles for NF-{kappa}B in these life stages. RNA-seq and GO analyses identify possible gene targets and biological functions of Co-NF-{kappa}B. We also show that three NF-{kappa}B-like proteins from the choanoflagellate Acanthoeca spectabilis (As) all consist of primarily the N-terminal conserved Rel Homology domain sequences of NF-{kappa}B, and lack C-terminal ANK repeats. All three As-NF-{kappa}B proteins constitutively enter the nucleus of human and Co cells, but differ in their DNA-binding and transcriptional activation activities. Furthermore, all three As-NF-{kappa}B proteins can form heterodimers, indicating that NF-{kappa}B diversified into multi-subunit families at least two times during evolution. Overall, these results present the first functional characterization of NF-{kappa}B in a taxonomic kingdom other than Animalia and provide information about the evolution and diversification of this biologically important transcription factor. SignificanceThese results represent the first functional characterization of the biologically important transcription factor NF-{kappa}B in a taxonomic kingdom other than Animalia. As such, they provide information on the evolutionary origins and basal diversification of NF-{kappa}B outside of metazoans. These results suggest that NF-{kappa}B plays life stage-specific roles in Capsaspora, the closest unicellular ancestor to all metazoans. Finally, the analysis of three NF-{kappa}B proteins in a single choanoflagellate indicates that choanoflagellates have subclasses of NF-{kappa}Bs, which can form heterodimers, suggesting that NF-{kappa}B subunit expansion and diversification has occurred at least twice in evolution.

cell biology↗

bioRxiv2022

The stationary phase-specific sRNA fimR2 is a multifunctional regulator of bacterial motility, biofilm formation and virulence

Bacterial pathogens employ a plethora of virulence factors for host invasion, and their use is tightly regulated to maximize infection efficiency and manage resources in a nutrient-limited environment. Here we show that during Escherichia coli stationary phase the small non-coding RNA fimR2 regulates fimbrial and flagellar biosynthesis at the post-transcriptional level, leading to biofilm formation as the dominant mode of survival under conditions of nutrient depletion. fimR2 interacts with the translational regulator CsrA, antagonizing its functions and firmly tightening control over motility and biofilm formation. Generated through RNase E cleavage, fimR2 regulates stationary phase biology independently of the chaperones Hfq and ProQ. The Salmonella enterica version of fimR2 induces effector protein secretion by the type III secretion system and stimulates infection, thus linking the sRNA to virulence. This work reveals the importance of bacterial sRNAs in modulating various aspects of bacterial physiology including stationary phase and virulence. HighlightsO_LIfimR2 expression causes biofilm formation and alters bacterial outer membrane architecture C_LIO_LIfimR2 modulates CsrA activity and sequesters it from its targets C_LIO_LIThe Salmonella fimR2 variant is functional in E. coli C_LIO_LIfimR2 is generated through RNase E processing and enhances infectivity C_LI

molecular biology↗

bioRxiv2025

The role of the Trypanosoma cruzi enzyme L-threonine 3-dehydrogenase in combating stressful environments

Trypanosoma cruzi is a digenetic parasite that undergoes various transformations to complete its life cycle. Changes between hosts and vectors involve exposure to stressful environments, for which it has developed different strategies to cope with such stress. L-threonine 3-dehydrogenase (TDH) is a key enzyme in trypanosome metabolism, and several studies have shown that inhibiting TDH affects parasite survival. To understand the role of TDH in T. cruzi, we investigated its expression in different benznidazole (Bz)-resistant clones and overexpressed it in a Bz-susceptible clone. After overexpressing TDH and exposing it to reactive oxygen species (ROS), alkylating agents, and drugs such as Bz, we evaluated certain biological parameters. Our results show that TDH led to higher survival rates when exposed to H2O2 and increased tolerance to Bz. Moreover, the parasites were able to infect more cells, and their mitochondrial membrane potential ({Psi}m) remained unchanged, both of which are linked to higher tolerance to ROS. Finally, parasites overexpressing TDH were less vulnerable to genetic damage caused by agents such as MMS and gamma radiation. Overall, our results demonstrate that TDH, a key enzyme in threonine metabolism, helps combat stressful environments and, under certain experimental conditions, supports the survival of parasites.

molecular biology↗

bioRxiv2019

The proteome of small urinary extracellular vesicles after kidney transplantation as an indicator of renal cellular biology and a source for markers predicting outcome

Kidney transplantation is the preferred renal replacement therapy available. Yet, the biological processes during and after kidney transplantation and how they translate into the overall functional graft outcome are insufficiently understood. Recent developments in the field of extracellular vesicle research allow the deeper exploitation of this non-invasive source. We separated small urinary extracellular vesicles (suEVs) throughout the course of living donor kidney transplantation. SuEVs were collected longitudinally from both the donor and the recipient in 22 living donor kidney transplantations. Unbiased proteomic analysis revealed specific temporal patterns of suEV proteins indicative of the cellular processes involved in the allografts response after transplantation with proteins playing a role in complement activation being among the most dynamically regulated components. Using a leave-one-out cross validation model, we identified potential prognostic markers of kidney function at 1 year after transplantation. One of the proteins identified - phosphoenol pyruvate carboxykinase (PCK2) - could be confirmed in an independent validation cohort of another 22 donor-recipient pairs using targeted mass spectrometry. This study sheds the light on early molecular processes during the course of kidney transplantation and shows the future potential of suEVs as a source of biomarkers in this setting. The data set is provided as a unique resource directly accessible through an online tool that allows dynamic interrogation of this first comprising suEV proteome atlas after kidney transplantation. One Sentence SummaryThis study represents the first atlas of the proteomic changes in small urinary extracellular vesicles throughout living donor kidney transplantation identifying PCK2 abundance as a biomarker for renal function 12 months after transplantation

molecular biology↗

bioRxiv2026

Microbial Antioxidants Reduce ROS In Human Skin Cells Under Oxidative Stress

Reactive oxygen species (ROS) play a dual role in cellular homeostasis, but excessive levels of ROS lead to oxidative stress, accelerating skin aging. Environmental stressors like UV radiation induce ROS overproduction, overwhelming endogenous antioxidant defenses and causing cellular damage. While the skin possesses an intrinsic antioxidant network that provides moderate protection, excessive oxidative stress can trigger inflammatory responses, thereby necessitating exogenous antioxidant intervention. Microbe-derived antioxidants (MA), produced via probiotic fermentation of sea buckthorn and chestnut rose, have shown promise in mitigating ROS-induced damage. In this study, we evaluated two MA formulations, MA1 and MA2, for their ability to scavenge free radicals and alleviate hydrogen peroxide (H2O2)-induced oxidative stress in human dermal fibroblasts (HDF) and dermal papilla cells (HDP). Both formulations displayed dose-dependent DPPH radical scavenging activity and enhanced cell viability at low concentrations. Under H2O2-induced oxidative stress, MA1 and MA2 effectively restored intracellular ROS to baseline levels, demonstrating significant cytoprotective effects. UHPLC-MS/MS profiling identified 12 compounds shared by both formulations, and Gene Ontology Biological Process enrichment analysis revealed that their associated target genes were significantly enriched in antioxidant-related pathways. Five compounds--adenosine, citric acid, 5-hydroxymethylfurfural, myricetin, and phenylalanine--emerged as key contributors to the observed antioxidative effects. Together, these findings highlight the potential of fermented microbial antioxidants to re-establish redox homeostasis in human skin cells and support their further development as therapeutic or cosmetic interventions targeting oxidative stress and skin aging. Given the heightened oxidative sensitivity of aged fibroblasts, MAs ability to alleviate ROS may offer novel therapeutic strategies against skin aging and related pathologies.

molecular biology↗

bioRxiv2023

Harnessing the endogenous Type I-C CRISPR-Cas system for genome editing in Bifidobacterium breve

Bifidobacterium breve, one of the main bifidobacterial species colonizing the human gastrointestinal tract in early life, has received extensive attention for its purported beneficial effects on human health. However, exploration of the mode of action of such beneficial effects exerted by B. breve is cumbersome due to the lack of effective genetic tools, which limits its synthetic biology application. Given the widespread presence of endogenous CRISPR-Cas systems in B. breve, the current study developed an endogenous CRISPR-based gene editing toolkit for genetic manipulation of B. breve. Deletion of the gene coding uracil phosphoribosyl-transferase (upp) was achieved in two different B. breve strains using this system. In addition, translational termination of uracil phosphoribosyl-transferase was successfully achieved in B. breve FJSWX38M7 by single-base substitution of the upp gene and insertion of three stop codons. The gene encoding linoleic acid isomerase (bbi) in B. breve, being a characteristic trait, was deleted after plasmid curing, which rendered it unable to convert linoleic acid into conjugated linoleic acid, demonstrating the feasibility of successive editing. This study expanded the gene manipulation toolkit of B. breve and provides a reference for functional genome editing and analysis using an endogenous CRISPR-Cas system in Bifidobacterium. ImportanceThe lack of effective genetic tools for Bifidobacterium breve is an obstacle to studying the molecular mechanisms of its health-promoting effects, hindering the development of next-generation probiotics. Here, we introduce a gene editing method based on the endogenous CRISPR-Cas system, which can achieve gene deletion, single base substitution, gene insertion and continuous gene editing in B. breve. This study will promote the excavation of functional genes and elucidation of molecular mechanisms of B. breve.

molecular biology↗

bioRxiv2024

Deletion of an sRNA primes development in a multicellular bacterium

ABSTRACTSmall non-coding RNAs (sRNAs) are essential in regulating gene expression during many biological processes. The myxobacteria gene pxr encodes an sRNA known to block fruiting-body development, an aggregative multicellular process triggered by starvation. Deletion of pxr allows Myxococcus xanthus cells to develop in the presence of nutrients. However, potential Pxr binding targets and most genes regulated by Pxr remain unknown. Here, we found that the absence of pxr expression dramatically alters the temporal dynamics of development, thus suggesting an important new role of this sRNA in myxobacterial ecology. We transcriptionally profiled vegetative cells of M. xanthus strains possessing vs lacking pxr and found that over half of the genes impacted by pxr deletion during growth are linked to development, including known and potentially novel critical regulators. Many other genes are associated with general metabolic processes, which Pxr regulates positively. Our study discovers new phenotypic effects of Pxr regulation of likely ecological importance, identifies the suite of genes this sRNA controls during vegetative growth, reveals a previously unknown developmental regulator and provides new insights into the early molecular regulation of myxobacterial development.

molecular biology↗

bioRxiv2023

DMS-MapSeq Analysis of Antisense Oligonucleotide Binding to lncRNA PANDA

While various methods exist for examining and visualizing the structure of RNA molecules, dimethyl sulfate-mutational profiling and sequencing (DMS-MaPseq) stands out for its simplicity and versatility. This technique has proven effective for studying RNA structures both in vitro and in complex biological settings. Weve updated the protocol for using DMS-MaPseq, and it can also be employed to identify the binding of antisense oligonucleotides (ASOs) to RNA. By applying this updated protocol, we successfully characterized the structural ensemble of the HIV1 Rev Response Element (RRE), along with its two alternative structures. The findings align with previously published research. Additionally, we resolved the structure of the long non-coding RNA PANDA, which was previously unknown. Moreover, we used PANDA as a basis for designing ASOs and confirmed their binding through a substantial decrease in DMS-reactivities at the anticipated ASO binding locations.

molecular biology↗

bioRxiv2024

Cross-expression analysis reveals patterns of coordinated gene expression in spatial transcriptomics

Spatial transcriptomics promises to transform our understanding of tissue biology by molecularly profiling individual cells in situ. A fundamental question they allow us to ask is how nearby cells orchestrate their gene expression. Rather than focus on how these cells (samples) communicate with each other, we reframe the problem to investigate how genes (features) coordinate their expression between neighboring cells. To study these phenomena - called cross-expression - we compare all genes to find pairs that coordinate their expression between adjacent cells, thereby avoiding curating gene lists or annotating cell types. Our end-to-end method recovers ligand-receptor pairs as cross-expressing genes and finds gene combinations that mark anatomical regions, complementing marker gene-based region annotation. Leveraging the overlapping genes across different panels, we use multiple atlas-scale adult mouse brain datasets (~25 million cells, 695 samples, 8 technologies) to create an integrated, meta-analytic cross-expression network, whose communities are enriched in spatial processes such as synaptic signaling and G protein coupled receptor activity. Highlighting cross-expressions biological utility, our network shows that genes Drd1 and Gpr6, which are individually implicated in Parkinsons disease (PD) and are being pursued as therapeutic targets, are cross-expressed within the striatum, hinting at their joint role in PD pathophysiology. We provide an efficient R package (https://github.com/gillislab/CrossExpression/) to computationally analyze and visually explore cross-expression patterns, which allow us to better understand how genes coordinate their expression in space to perform tissue-level functions.

bioinformatics↗

bioRxiv2026

Convergent Multimodal Evidence of Cortical Excitation-Inhibition Imbalance in Psychosis

Psychosis is increasingly understood as a disorder of disrupted cortical excitation-inhibition balance, yet robust non-invasive translational biomarkers remain lacking. The resting-state fMRI Hurst exponent (HE) and EEG aperiodic spectral exponent are promising complementary biomarkers, with lower values in each proposed to reflect a shift towards cortical hyperexcitability, but they have not been jointly examined in psychosis, and the spatial and molecular architecture of HE alterations remains poorly defined. We therefore tested for convergent systems-level signatures across independent cohorts and modalities, using resting-state fMRI (107 patients, 53 controls) and EEG (547 patients, 363 controls). Whole-brain and regional HE were estimated using wavelet methods, and EEG aperiodic exponents were quantified using spectral parameterisation. Compared with healthy controls, individuals with psychosis showed reduced whole-brain HE and widespread regional reductions. Regional HE case-control differences were associated with cortical gene-expression patterns, with enrichment for potassium channel and GABA receptor pathways, and correlated with noradrenergic, muscarinic, serotonergic, glutamatergic and dopaminergic receptor density maps, but not with cortical thickness or symptom or cognitive measures. In the independent EEG cohort, psychosis was similarly associated with a reduced aperiodic spectral exponent. Together, these findings provide cross-modal evidence for altered cortical resting-state dynamics in psychosis, consistent with a shift towards cortical hyperexcitability. Integration with receptor-density and transcriptomic maps implicates biologically plausible molecular pathways and supports HE and EEG aperiodic activity as scalable translational biomarkers in psychosis.

neuroscience↗

bioRxiv2021

Multiple nucleotide polymorphism DNA markers for the accurate evaluation of genetic variations

DNA markers are an essential tool for the detection and evaluation of genetic variations, a central theme in genetics and biology. Effective markers must be highly reproducible, polymorphic, accurate and efficient to profile. We developed multiple dispersed nucleotide polymorphism (MNP) DNA marker and an efficient MNP genotyping method called MNP-Seq. The MNP marker was 17.48% more polymorphic than the highly polymorphic marker of microsatellites on a collection of hybrid rice plants. When applied to genotype more than 80,000 individual MNP markers of diploid rice and polyploidy hybrid cotton varieties which were notoriously difficult to genotype accurately, MNP-Seq finished in two days and achieved accuracies of 99.999% and 99.988%, respectively. We adopted MNP-Seq to reveal the ubiquitous, albeit subtle and neglected, genetic heterogeneities in homonyms of Nipponbare rice, a popular model organism for plant biology. This result raised a question on the consistency of the published results using the model plant. We also used MNP-Seq to accurately and efficiently determine the identities of plant varieties, a key but difficult problem for the protection of plant intellectual property rights. While being applied to plants in the current study, the MNP marker and MNP-Seq are general and readily applicable to similar problems in animals and micro-organisms.

molecular biology↗

bioRxiv2022

RNA m6A and 5hmC regulate monocyte and macrophage gene expression programs

BackgroundRNA modifications are essential for the establishment of cellular identity. Although increasing evidence indicates that RNA modifications regulate the innate immune response, their role in monocyte-to-macrophage differentiation and polarisation is unclear. To date, most studies have focused on m6A, while other RNA modifications, including 5hmC, remain poorly characterised. The interplay between different RNA modifications that may occur in specific cellular contexts remains similarly unexplored. ResultsWe profiled m6A and 5hmC epitranscriptomes, transcriptomes, translatomes and proteomes of monocytes and macrophages at rest and pro- and anti-inflammatory states. We observed that decreased expression of m6A and 5hmC writers, METTL3 and TET-enzymes respectively, facilitated monocyte-to-macrophage differentiation. Despite a global trend of m6A and 5hmC loss during macrophage differentiation, enrichment of m6A and/or 5hmC on specific categories of transcripts essential for macrophage differentiation positively correlated with their expression and translation. m6A and 5hmC mark and are associated with the expression of transcripts with critical functions in pro- and anti-inflammatory macrophages. Notably, we also discovered the coexistence of m6A and 5hmC marking alternatively-spliced isoforms and/or opposing ends of the untranslated regions (UTR) of transcripts with key roles in macrophage biology. In specific examples, RNA 5hmC controls the decay of transcripts independently of m6A. ConclusionsThis study: i) uncovers m6A, 5hmC and their writer enzymes as regulators of monocyte and macrophage gene expression programs and ii) provides a comprehensive dataset to interrogate the role of RNA modifications in a plastic system. Altogether, this work sheds light on the role of RNA modifications as central regulators of effector cells in innate immunity.

molecular biology↗

bioRxiv2025

Detection of archaeal- and prokaryotic-like ribosome exit tunnels within eukaryotic kingdoms

The ribosome exit tunnel is a critical sub-compartment that actively regulates the folding and dynamics of nascent polypeptide chains during protein translation. In this study, we systematically examined tunnel structures of 725 ribosome models obtained through cryo-EM and X-ray crystallography, to quantify structural variations across different species and biological domains. Hierarchical clustering revealed significant geometric differences between prokaryotic and eukaryotic ribosomes, with a surprising discovery: six eukaryotic protist species display tunnel structures remarkably similar to those of archaea and bacteria. By analyzing the sequences and structures of ribosomal components forming the tunnel walls, we identified four specific sequence modifications in ribosomal proteins and ribosomal RNAs (rRNA) responsible for these unique geometric variations, and detected these modifications in additional protist species lacking existing 3D structural data. Overall, our findings highlights some complex evolutionary mechanisms governing ribosomal protein and large subunit rRNA, providing novel insights into the tunnels regulatory role in protein translation.

molecular biology↗

bioRxiv2021

Notch-dependent DNA cis-regulatory elements and their dose-dependent control of C. elegans stem cell self-renewal

A long-standing biological question is how DNA cis-regulatory elements shape transcriptional patterns during metazoan development. The use of reporter constructs, cell culture and computational modeling has made enormous contributions to understanding this fundamental question, but analysis of regulatory elements in their natural developmental context is an essential but rarely used complement. Here, we edited Notch-dependent cis-regulatory elements in the endogenous C. elegans sygl-1 gene, which encodes a key stem cell regulator. We then analyzed the in vivo consequences of those mutations - on both gene expression (nascent transcripts, mRNA, protein) and stem cell maintenance. Mutation of a single element in a three-element homotypic cluster reduced expression as well as stem cell pool size by about half, while mutation of two elements essentially abolished them. We find that LBS number and LBS neighborhood are both important to activity: elements on separate chromosomes function additively, while elements in the same cluster act synergistically. Our approach of precise CRISPR/Cas9 gene editing coupled with quantitation of both molecular and biological readouts establishes a powerful model for in vivo functional analyses of DNA cis-regulatory elements. Summary statementNotch-dependent DNA cis-regulatory elements work together in their developmental context to shape a transcriptional gradient, control stem cell pool size, and govern differentiation onset.

developmental biology↗

bioRxiv2023

3D electron microscopy of the Leishmania mexicana cell cycle: Patterns of organelle duplication and segregation and their implications for parasite biology

The unicellular parasite Leishmania has a precisely defined cell architecture that is inherited by each subsequent generation, requiring a highly coordinated pattern of duplication and segregation of organelles and cytoskeletal structures. A framework of nuclear division and morphological changes is known from light microscopy, yet this has limited resolution and the intrinsic organisation of organelles within the cell body and their manner of duplication and inheritance is unknown. Using volume electron microscopy approaches, we have produced three-dimensional reconstructions of different promastigote cell cycle stages to give a spatial and quantitative overview of organelle positioning, division and inheritance. The first morphological indications seen in our dataset that a new cell cycle had begun were the assembly of a new flagellum, the duplication of the contractile vacuole and the increase in volume of the nucleus and kinetoplast. We showed that the progression of the cytokinesis furrow created a specific pattern of membrane indentations and sub-pellicular microtubule organisation indicates that is likely a preferred site of new microtubule insertion. The daughter cells retained these indentations in their cell body for a period post-abscission. By comparing cultured and sand fly derived promastigotes, we found an increase in the number and overall volume of lipid droplets in the promastigotes from the sand fly, reflecting a change in their metabolism to ensure transmissibility to the mammalian host. Our insights into the cell cycle mechanics of Leishmania will be invaluable for future molecular cell biology analyses of these important parasites.

cell biology↗

bioRxiv2020

Overview of the expression of key regeneration genes in embryo development and matured tissues in Axolotl (Ambystoma mexicanum)

The axolotl is a Mexican endangered species with the capability to perform tissue regeneration in amputated extremities. Being an important research model, the complete genome of the Axolotl was sequenced in 2018 for the first time, revealing an enormous genome: the largest of any animal ever sequenced, and about 10 times larger than the human genome, a new landmark achievement in biology research. In this report, we collected 70 known genes that play an important role in tissue regeneration and searched for their expression during embryo development, regeneration, and in 6 adult tissues: the heart, liver, gills, front leg, rear leg, and tail. We observe those 70 genes expression levels in the 3 conditions and approximately 3 genes seem to be expressed exclusively in regeneration. This report displays a few insights on how this marvelous species can modulate its regenerative capabilities. There is still much more to explore with the Axolotl. Further research into their regenerative capabilities could provide researchers with the perspicacity to possibly accomplish human limb regeneration.

molecular biology↗