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bioRxiv2026

RNA-binding is the essential biological function of the Drosophila protein Brat

Brain tumor (Brat) is a Drosophila TRIM-NHL protein required for embryogenesis and neural stem cell differentiation. Although structural and biochemical studies established that the Brat NHL domain specifically binds RNA, the in vivo requirement for this activity has not been directly tested. Here, we used structure-guided mutagenesis and genome engineering to determine whether RNA recognition is essential for Brat function during development. The direct interaction between Brats NHL domain and RNA containing Brat Binding Sites (BBS) can be abolished by alanine substitution of three separate residues on the NHL surface. We introduced these point mutations into the endogenous brat locus by CRISPR-mediated Scarless Gene Editing to generate three independent RNA-binding defective mutant (RBDmt) alleles. Complementation tests demonstrated that each allele behaves as a strong loss-of-function mutation: homozygotes and hemizygotes are inviable, and RBDmt alleles fail to complement classical brat null and hypomorphic alleles. Lethal phase analysis revealed death predominantly during late larval and pupal stages, consistent with known brat alleles. Consistent with the namesake brat phenotype, RBDmt larval brains exhibited widespread expression of neuroblast markers and a marked reduction of neuronal differentiation. In embryos, these alleles failed to complement female sterile brat alleles and recapitulated characteristic abdominal segmentation defects. Finally, RT-qPCR showed increased expression of endogenous Brat target mRNAs in mutant larvae, consistent with loss of Brat-mediated repression. Together, these results demonstrate that direct RNA binding is the essential molecular activity of Brat and that post-transcriptional regulation of Brat target mRNAs underlies its critical roles across development.

molecular biology↗

bioRxiv2023

Methylation Array Signals are Predictive of Chronological Age Without Bisulfite Conversion

DNA methylation data has been used to make "epigenetic clocks" which attempt to measure chronological and biological aging. These models rely on data derived from bisulfite-based measurements, which exploit a semi-selective deamination and a genomic reference to determine methylation states. Here, we demonstrate how another hallmark of aging, genomic instability, influences methylation measurements in both bisulfite sequencing and methylation arrays. We found that non-methylation factors lead to "pseudomethylation" signals that are both confounding of epigenetic clocks and uniquely age predictive. Quantifying these covariates in aging studies will be critical to building better clocks and designing appropriate studies of epigenetic aging.

molecular biology↗

bioRxiv2025

TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination

The Androgen Receptor (AR) is a ligand-dependent transcription factor that drives prostate cancer development and progression. Although, a detailed effect on AR biology has been described for a number of interacting proteins, many AR coregulators remain to be characterized in relation to their distinct impact on AR function. Here, we describe TRIM33 as a conserved AR-interactor across multiple prostate cancer cell lines. We observed that TRIM33 and AR share overall chromatin interaction profiles, in which TRIM33 is involved in downstream responsive transcriptomic output. In contrast to prior reports, we show that TRIM33 does not impact AR protein stability, but instead propose a model in which TRIM33 facilitates maximal AR activity by interfering with H2BK120 ubiquitination levels.

molecular biology↗

bioRxiv2025

Age-based approach to characterize the dynamics of cellular processes

Cells continuously produce and degrade multiple small and large molecules, essential for maintaining homeostasis. The study of these dynamics has gained momentum since the development of pulse-chase and wash-in/out methods, utilizing fluorescent or isotopic labeling of cellular components to assess properties such as turnover rates or half-lives. However, standard analyses of these experiments often depend on simplifications such as the homogeneity of analyzed molecules or their immediate labeling, which do not always hold. Here, we present a rigorous analytical framework that interprets the readouts of dynamic labeling experiments as the distribution of metabolic ages, defined as the time that molecules have spent within a cell, and show that metabolic ages can be quantified by dynamic labeling with minimal assumptions. Using age-based interpretation, we demonstrate how the experimentally observed labeling dynamics is connected to a variety of dynamic parameters including half-lives, decay rates, and residence times and how these interpretations are affected by the conditions of delayed input or complex degradation patterns. To aid in the experimental quantification of dynamic parameters, we introduce a compartmental model framework including an open-source software package. We illustrate the frameworks practical utility by quantifying dynamic parameters and determining the kinetic pool structure of budding yeast proteins at optimal and suboptimal growth temperatures. Significance StatementTo be functional, cells must balance the production and degradation of biological molecules. This is often studied by labeling newly-made molecules with isotopic or fluorescent labels. However, determining parameters of these processes, such as degradation rates, is not easy and is challenged by non-instantaneous labeling and complex degradation patterns. We describe a generic framework for interpreting the results of dynamic labeling experiments based on the concept of metabolic age, defined as the time since a molecule entered the metabolic system. By analyzing the effects of heat stress on protein stability in yeast, we illustrate how this framework and its implementation in a custom opensource package enable us to standardize the determination of various dynamic parameters of metabolism.

molecular biology↗

bioRxiv2026

A Multi-Modal AI/ML-based Framework for Protein Conformation Selection and Prediction in Drug Discovery Applications

The development of pharmaceutical drugs is a time-intensive and costly process, with more than 90% of drug candidates failing during preclinical or clinical testing. A major challenge lies in accurately predicting protein-ligand interactions, especially given that traditional computational methods often rely on a single protein conformation, failing to capture biologically relevant structural variability. To address this, we present an AI/ML-based multi-modal framework based on Graph Convolutional Network (GCN) that integrates both global and local protein descriptors to classify binding and non-binding conformations more effectively. Global descriptors capture overarching physico-chemical and structural properties of proteins, while local descriptors--such as pharmacophores--provide site-specific information crucial for modeling ligand interactions. Our GCN based approach demonstrates that integrating local and global structural perspectives significantly improves predictive accuracy and robustness. By enabling more reliable protein conformation classification, this work contributes toward scalable, AI-driven drug discovery--an increasingly critical goal in response to global health challenges.

molecular biology↗

bioRxiv2020

Signal and noise in circRNA translation

Within recent years, circular RNAs (circRNAs) have been an attractive new field of research in RNA biology and disease. Consequently, numerous studies have been published towards the disclosure of circRNA biogenesis and function. Initially, circRNAs were described as a subclass of cytoplasmic non-coding RNA, however, a few recent observations have proposed that circRNAs may instead be templates for protein production. The extent to which this is the case is currently debated, and therefore using rigorous data analysis and proper experimental setups is instrumental to settle the current controversies. Here, the conventional experiments used for detecting circRNA translation are outlined, and guidelines to distinguish signal from the inherent noise are discussed. While these guidelines are specific for circRNA translation, most also apply to all other aspects of non-canonical translation.

molecular biology↗

bioRxiv2025

NPAS2 attenuates VSMC phenotypic switching in ascending thoracic aortic aneurysm via LPCAT3/PC-PUFA2S-mediated ferroptosis

Ascending thoracic aortic aneurysm (ATAA) is a life-threatening disorder with limited therapeutic options, critically linked to vascular smooth muscle cell (VSMC) phenotypic switching. Neuronal PAS Domain Protein 2 (NPAS2), a circadian rhythm-related transcription factor, regulates diverse physiological processes. However, the biological functions and underlying regulatory mechanisms of NPAS2 in VSMCs during ATAA pathogenesis remain to be elucidated. NPAS2 expression decreased in ATAA patients, PDGF-BB-treated HASMCs and BAPN-administrated mice. NPAS2 depletion facilitated VSMC phenotype switching. VSMC-specific NPAS2 knockout (NPAS2SMKO) mice exhibited aggravated ATAA. Mechanistically, NPAS2 depletion attenuates its transcriptional repression of LPCAT3, subsequently elevating the accumulation of phosphatidylcholines with two polyunsaturated fatty acyl chains (PC-PUFA2S), thereby promoting ferroptosis-induced VSMC phenotype switching and accelerating ATAA progression. Targeting NPAS2 represents a potential therapeutic strategy for ATAA treatment.

molecular biology↗

bioRxiv2018

Aspergillus niger citrate exporter revealed by comparison of two alternative citrate producing conditions

Currently, there is no consensus regarding the mechanism underlying Aspergillus niger citrate biosynthesis and secretion, although it is amongst the most studied biotechnological production processes. Carbon excess relative to various other medium constituents is key, but the complex interplay between the limiting factors required for extracellular citrate accumulation remains elusive. It is thought that one of the industrial bottlenecks for citrate production is citrate export, however, no A. niger citrate exporter has yet been identified. Here, we show that the phenotype of increased extracellular citrate accumulation can have fundamentally different underlying mechanisms, depending on how this response is triggered, and that combining gene expression analyses of the different conditions can lead to the compilation of a shortlist of the most promising citrate exporter candidates. Specifically, we found that varying the amount and type of supplement of an arginine auxotrophic A. niger strain shows down-regulation of citrate metabolising enzymes in the condition in which more citrate is accumulated extracellularly. This contrasts with the transcriptional adaptations triggered by iron limitation, which also induces increased A. niger citrate production. By combining data obtained from these two manners of inducing comparatively high extracellular citrate accumulation, we were able to compile a shortlist of the most likely citrate transporter candidates. Two of the most promising candidates were tested in the yeast Saccharomyces cerevisiae, one of which showed the ability to secrete citrate. Deletion of the endogenous A. niger gene encoding the corresponding transporter abolished the ability of this fungus to secrete citrate. Instead, under conditions that usually favour A. niger citrate production, we found increased accumulation of extracellular oxalate. Our findings provide steps in untangling the complex interplay of different mechanisms underlying A. niger citrate accumulation, and we identify, for the first time, a fungal citrate exporter, offering a valuable tool for improvement of A. niger as biotechnological cell-factory for organic acid production.\n\nAuthor SummaryCitrate is widely applied as acidifier, flavouring and chelating agent. Industrial citrate production currently relies on the filamentous fungus Aspergillus niger. Although the industrial production process using A. niger has vastly improved since initiated almost 100 years ago, citrate export remains a bottleneck. Here, we studied the gene expression pattern of A. niger under various citrate producing conditions. Using these expression patterns and different computational approaches, we compiled a shortlist of putative citrate exporter candidates. In this way, we were able to identify a gene encoding a transporter protein capable of citrate export. We show that the yeast Saccharomyces cerevisiae, normally a citrate non-producer, secretes detectable amounts of citrate when harbouring this gene. In addition, we verify the biological function of this gene in A. niger itself, as removing this gene resulted in a citrate non-producing phenotype, which is atypical for this fungus. This finding is particularly exciting, as it is the first identification of a eukaryotic citrate exporter. With this, we not only provide a tool for improvement of industrial citrate production, but knowledge of this gene should help develop new methods for improvement of A. niger as biotechnological cell-factory for the production of other organic acids.

molecular biology↗

bioRxiv2021

Zika virus infection drives epigenetic modulation of immunity by the histone acetyltransferase CBP of Aedes aegypti

Epigenetic mechanisms are responsible for a wide range of biological phenomena in insects, controlling embryonic development, growth, aging and nutrition. Despite this, the role of epigenetics in shaping insect-pathogen interactions has received little attention. Gene expression in eukaryotes is regulated by histone acetylation/deacetylation, an epigenetic process mediated by histone acetyltransferases (HATs) and histone deacetylases (HDACs). In this study, we explored the role of the Aedes aegypti histone acetyltransferase CBP (AaCBP) after infection with Zika virus (ZIKV), focusing on the two main immune tissues, the midgut and fat body. We showed that the expression and activity of AaCBP could be positively modulated by blood meal and ZIKV infection. Nevertheless, Zika-infected mosquitoes that were silenced for AaCBP revealed a significant reduction in the acetylation of H3K27 (CBP target marker), followed by downmodulation of the expression of immune genes, higher titers of ZIKV and lower survival rates. Importantly, in Zika-infected mosquitoes that were treated with sodium butyrate, a histone deacetylase inhibitor, their capacity to fight virus infection was rescued. Our data point to a direct correlation among histone hyperacetylation by AaCBP, upregulation of antimicrobial peptide genes and increased survival of Zika-infected-A. aegypti. Author summaryPathogens have coevolved with mosquitoes to optimize transmission to hosts. As natural vectors, mosquitoes are permissive to and allow systemic and persistent arbovirus infection, which intriguingly does not result in dramatic pathological sequelae that affect their lifespan. In this regard, mosquitoes have evolved mechanisms to tolerate persistent infection and develop efficient antiviral strategies to restrict viral replication to nonpathogenic levels. There is a great deal of evidence supporting the implication of epigenetics in the modulation of the biological interaction between hosts and pathogens. This study reveals that Zika virus infection positively modulates the expression and activity of A. aegypti histone acetyltransferase CBP (AaCBP). This study shows that AaCBP plays a role in the activation of immune-responsive genes to limit Zika virus replication. This first description that Zika virus infection has epigenomic consequences in the regulation of A. aegypti immunity opens a new avenue for research on mosquito factors that can drive vector competence.

molecular biology↗

bioRxiv2024

The ABCF ATPase New1 resolves translation termination defects associated with specific tRNAArg and tRNALys> isoacceptors in the P site

The efficiency of translation termination is determined by the nature of the stop codon as well as its context. In eukaryotes, recognition of the A-site stop codon and release of the polypeptide are mediated by release factors eRF1 and eRF3, respectively. Translation termination is modulated by other factors which either directly interact with release factors or bind to the E-site and modulate the activity of the peptidyl transferase center. Previous studies suggested that the Saccharomyces cerevisiae ABCF ATPase New1 is involved in translation termination and/or ribosome recycling, however, the exact function remained unclear. Here, we have applied 5PSeq, single-particle cryo-EM and readthrough reporter assays to provide insight into the biological function of New1. We show that the lack of New1 results in ribosomal stalling at stop codons preceded by a lysine or arginine codon and that the stalling is not defined by the nature of the C-terminal amino acid but rather by the identity of the tRNA isoacceptor in the P-site. Collectively, our results suggest that translation termination is inefficient when ribosomes have specific tRNA isoacceptors in the P-site and that the recruitment of New1 rescues ribosomes at these problematic termination contexts.

molecular biology↗

bioRxiv2020

Re-analysis of SARS-CoV-2 infected host cell proteomics time-course data by impact pathway analysis and network analysis. A potential link with inflammatory response.

The disease known as coronavirus disease 19 (COVID-19), potentially caused by an outbreak of the severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) in Wuhan, China, has hit the world hard, and has led to an unprecedent health and economic crisis. In order to develop treatment options able to stop or ameliorate SARS-CoV-2 effects, we need to understand the biology of the virus inside cells, but this kind of studies are still scarce. A recent study investigated translatome and proteome host cell changes induced in vitro by SARS-CoV-2. In the present study, we use the publicly available proteomics data from this study to re-analyze the mechanisms altered by the virus infection by impact pathways analysis and network analysis. Proteins linked to inflammatory response, but also proteins related to chromosome segregation during mitosis, were found to be regulated. The up-regulation of the inflammatory-related proteins observed could be linked to the propagation of inflammatory reaction and lung injury that is observed in advanced stages of COVID-19 patients.

molecular biology↗

bioRxiv2025

γ-Amino Carboxylic Acid Modification Enhances the Efficacy of PNAs Targeting miR-221-3p in A549 Cells

Peptide nucleic acids (PNAs) are versatile tools for diagnostic and therapeutic applications, including gene regulation and miRNA targeting. However, their therapeutic potential is often limited by challenges such as biological efficacy. To address this, PNAs offer a key advantage over other nucleic acids--their ease of modification, which allows for enhanced properties. In this study, we introduced a novel{gamma} -amino carboxylic acid ({gamma}-ACA) modification to PNAs targeting miR-221-3p, a key miRNA implicated in various pathological processes. The modified PNAs showed significantly improved binding affinity to their targets and more efficient inhibition of miR-221-3p expression compared to unmodified PNAs in A549 cells, leading to effective regulation of downstream gene and protein expression. These results highlight the potential of{gamma} -modified PNAs as a platform for developing miRNA-targeted therapeutics.

molecular biology↗

bioRxiv2025

Modulating MyoD1 dosage activates alternate cell fate beyond myogenic differentiation

Transcription factor (TF) upregulation accompanies many cellular state transitions, yet how increased TF abundance impacts gene regulation remains unclear. Two broad models are often invoked, whereby higher TF levels amplify the expression of pre-existing target genes, or, by mass-action binding, expand genome engagement and regulation to lower-affinity sites. We sought to elucidate how these two regulatory modes contribute to cell differentiation in a well characterized myogenic system by upregulating the expression of the myogenic TF MyoD1 in C2C12 myoblasts. Unexpectedly, elevated MyoD1 levels impaired myoblast fusion (a hallmark of myogenic differentiation), yet enabled robust contraction in myotubes that did form. Live-cell single-molecule imaging and CUT&RUN profiling revealed that elevated MyoD1 dosage increased total genome-wide chromatin binding and broadened genome occupancy by preferentially engaging lower-affinity sites. Integrating CUT&RUN with RNA-seq experiments linked expanded MyoD1 binding to upregulation of cell adhesion genes. Cell mixing and fractionated RNA-seq experiments supported a two-population model in which an adhesion-gene-upregulated, unfused myoblast population supported contraction of myotubes formed by fusion-competent cells. Ectopic expression of several individual MyoD1-upregulated cell adhesion genes was sufficient to recapitulate the "off script" myotube contraction phenotype. Together, these results support a MyoD1 dose-dependent "spillover" model, in which increased TF abundance broadens cis-regulatory engagement and produces distinct cell differentiation outcomes. Significance StatementTranscription factor dosage is a central control knob in many biological and disease-associated cell state transitions, but its range of gene regulatory consequences are poorly understood. By inducibly elevating MyoD1 expression in C2C12 cells, we uncovered a paradoxical outcome: elevated MyoD1 levels suppressed myoblast fusion yet enabled robust myotube contraction. Elevated MyoD1 levels expanded MyoD1 genome occupancy through engagement of low-affinity sites and upregulated adhesion genes whose individual ectopic expression was sufficient to recapitulate the contraction phenotype. Mixing experiments indicated a non-cell-autonomous contribution from an adhesion-gene-high subpopulation that supported contraction of myotubes. Our results demonstrate that TF dosage can expand regulatory scope and yield qualitatively different differentiation outcomes.

molecular biology↗

bioRxiv2020

Meta-analysis of transcriptomes of SARS-Cov2 infected human lung epithelial cells identifies transmembrane serine proteases co-expressed with ACE2 and biological processes related to viral entry, immunity, inflammation and cellular stress.

The COVID-19 pandemic resulting from the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which emerged in December 2019 in the Chinese city of Wuhan in the province Hubei has placed immense burden on national economies and global health. At present neither vaccination nor therapies are available although several antiviral agents such as remdesivir, originally an Ebola drug, nelfinavir, an HIV-1 protease inhibitor and other drugs such as lopinavir have been evaluated. Here, we performed a meta-analysis of RNA-sequencing data from three studies employing human lung epithelial cells. Of these one focused on lung epithelial cells infected with SARS-CoV-2. We aimed at identifying genes co-expressed with angiotensin I converting enzyme 2 (ACE2) the human cell entry receptor of SARS-CoV-2, and unveiled several genes correlated or inversely correlated with high significance, among the most significant of these was the transmembrane serine protease 4 (TMPRSS4). Serine proteases are known to be involved in the infection process by priming the virus spike protein. Pathway analysis revealed papilloma virus infection amongst the most significantly correlated pathways. Gene Ontologies revealed regulation of viral life cycle, immune responses, pro-inflammatory responses-several interleukins such as IL6, IL1, IL20 and IL33, IFI16 regulating the interferon response to a virus, chemo-attraction of macrophages, last and not least cellular stress resulting from activated Reactive Oxygen Species. We believe that this dataset will aid in a better understanding of the molecular mechanism(s) underlying COVID-19.

molecular biology↗

bioRxiv2020

An ancient satellite repeat controls gene expression and embryonic development in Aedes aegypti through a highly conserved piRNA

Tandem repeat elements such as the highly diverse class of satellite repeats occupy large parts of eukaryotic chromosomes. Most occur at (peri)centromeric and (sub)telomeric regions and have been implicated in chromosome organization, stabilization, and segregation1. Others are located more dispersed throughout the genome, but their functions remained largely enigmatic. Satellite repeats in euchromatic regions were hypothesized to regulate gene expression in cis by modulation of the local heterochromatin, or in trans via repeat-derived transcripts2,3. Yet, due to a lack of experimental models, gene regulatory potential of satellite repeats remains largely unexplored. Here we show that, in the vector mosquito Aedes aegypti, a satellite repeat promotes sequence-specific gene silencing via the expression of two abundant PIWI-interacting RNAs (piRNAs). Strikingly, whereas satellite repeats and piRNA sequences generally evolve extremely fast4-6, this locus was conserved for approximately 200 million years, suggesting a central function in mosquito biology. Tandem repeat-derived piRNA production commenced shortly after egg-laying and inactivation of the most abundant of the two piRNAs in early embryos resulted in an arrest of embryonic development. Transcriptional profiling in these embryos revealed the failure to degrade maternally provided transcripts that are normally cleared during maternal-to-zygotic transition. Our results reveal a novel mechanism in which satellite repeats regulate global gene expression in trans via piRNA-mediated gene silencing, which is fundamental to embryonic development. These findings highlight the regulatory potential of this enigmatic class of repeats.

molecular biology↗

bioRxiv2020

Comparative analysis of biological aspects of Leishmania infantum isolates

Leishmania infantum infantum (LII) is one of the species that causes visceral leishmaniasis (VL) in the Old World, while L. infantum chagasi (LIC), and is present in the New World. Few studies address the biological differences, as well as the behaviour of these strains during infection. These parasites live inside the cells of their hosts, continuously evading the microbicidal mechanisms and modulating the immune response of these cells. One of the mechanisms used by these protozoa involves the L-arginine metabolism. Given the importance of the understanding of differences between Leishmania species, as well as establishing a better murine model to study leishmaniases, the objectives of this work were to analyse the biological and molecular differences between two Leishmania infantum strains (LII and LIC) and the degree of susceptibility of mice with different genetic backgrounds to infection, as well as to understand the role of arginase (ARG)/nitric oxide synthase (NOS) in the parasite-host relationship. The infectivity in vivo and in vitro of LII and LIC was performed in BALB/c and Swiss Webster mice, as well the NOS and ARG activities. The LII strain showed more infective than the LIC strain both in vivo and in vitro. In animals infected by both strains, a difference in NOS and ARG activities occurred. In vitro, promastigotes of LII isolated from BALB/c and Swiss Webster mice showed higher ARG activity than the LIC during the growth curve, however, no difference was observed in intracellular NO production by promastigotes between these strains. A comparison of the sequences of the ARG gene was made and both strains were identical. However, despite the similarity, the strains showed different expression of this gene. It can be concluded that although L. chagasi strains are considered identical to L. infantum strains, both have different biological behaviour.

pathology↗

bioRxiv2020

Methylation of RNA Cap in SARS-CoV-2 captured by serial crystallography

The genome of the SARS-CoV-2 coronavirus contains 29 proteins, of which 15 are nonstructural. Nsp10 and Nsp16 form a complex responsible for the capping of mRNA at the 5' terminus. In the methylation reaction the S-adenosyl-L-methionine serves as the donor of the methyl group that is transferred to Cap-0 at the first transcribed nucleotide to create Cap-1. The presence of Cap-1 makes viral RNAs mimic the host transcripts and prevents their degradation. To investigate the 2'-O methyltransferase activity of SARS-CoV-2 Nsp10/16, we applied fixed-target serial synchrotron crystallography (SSX) which allows for physiological temperature data collection from thousands of crystals, significantly reducing the x-ray dose while maintaining a biologically relevant temperature. We determined crystal structures of Nsp10/16 that revealed the states before and after the methylation reaction, for the first time illustrating coronavirus Nsp10/16 complexes with the m7GpppAm2'-O Cap-1, where 2'OH of ribose is methylated. We compare these structures with structures of Nsp10/16 at 297 K and 100 K collected from a single crystal. This data provide important mechanistic insight and can be used to design small molecules that inhibit viral RNA maturation making SARS-CoV-2 sensitive to host innate response.

molecular biology↗

bioRxiv2025

Parkia javanica extracts exhibits tissue regeneration potential in Zebrafish (Danio rerio)

Parkia javanica is a medicinal plant acknowledged for its diverse pharmacological features, but its biological effects, like regeneration and wound-healing properties, in the zebrafish animal model (Danio rerio) is unexplored. The purpose of this study was to determine the caudal fin tissue regeneration and antioxidant potential in response to Parkia javanica fruit and bark extracts on Danio rerio. The Danio rerio caudal fin was amputated and subsequently was treated with Parkia javanica fruit and bark extracts at 0.346{micro}g/mL and 2.86{micro}g/mL respectively. The regenerative effects of Parkia javanica fruit and bark extracts were evaluated through morphological analysis and dorso-ventral patterning. Additionally, the antioxidant properties of Parkia javanica fruit and bark extracts, along with the mechanistic insights, were evaluated using qRT-PCR. We found that both the Parkia javanica fruit and bark extracts displayed substantial antioxidant capacity with upregulation of key genes like Cat and Sod1. Further, the extracts demonstrated significant fin regeneration compared to the control group. We observed that both the Parkia javanica fruit and bark extracts possess tissue regeneration properties by upregulating key genes, like Anxa2a, Anxa2b, and Wnt3a. All these findings provide novel insights into the molecular mechanisms underlying the tissue repair and regeneration effects of Parkia javanica fruit and bark extracts and may pave the way for the development of novel regenerative therapeutic strategies. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=128 SRC="FIGDIR/small/681930v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@9a579org.highwire.dtl.DTLVardef@14edd37org.highwire.dtl.DTLVardef@9d7addorg.highwire.dtl.DTLVardef@ed79da_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗