Biology subjects

Sen, A.

Publications and source records attributed to Sen, A..

At least 19 recordsLinked to original sources

bioRxiv2026

Engaging the host adaptive response to nutrient limitation delays cancer cachexia

Cancer cachexia is a debilitating wasting syndrome associated with involuntary weight loss, reduced appetite and food intake, adipose and muscle atrophy, and systemic inflammation with induction of a myriad of candidate cachexia factors. Using a multi-omic approach in a genetically engineered mouse model of lung cancer cachexia, we found that early circulating metabolic alterations preceded overt weight loss. Although both cachexia and fasting are characterized by a reduction in food intake, we show that the systemic metabolic changes in cachexia are distinct, indicating a lack of induction in the normal protective response to negative energy balance during cachexia. Cancer cachexia causes profound hepatic reprogramming, and activation of inflammatory programs, alongside muscle atrophy and elevation of circulating cytokines. However, targeting individual candidate cachectic factors such as IL-6, TNF-, GDF15, CCL2, LIF, and IL17A failed to rescue weight loss or prolong survival. In contrast, caloric restriction initiated prior to tumor induction elicited a program of protection during tumor progression that attenuated multi-tissue inflammatory and catabolic transcriptional responses, preserved lean mass, and prolonged survival. Together, these findings suggest that metabolic preconditioning broadly dampens systemic inflammation and delays the onset and progression of cancer cachexia.

cancer biology↗

bioRxiv2026

Molecularly Distinct Innexin Gap Junction Channels and Undocked Hemichannels Regulate Glia Morphology and Function in Caenorhabditis elegans

Glial cells across species orchestrate nervous system development, maintenance, and function through ionic and metabolic crosstalk. These cells express multiple gap junction and hemichannel components. However, the mechanisms by which glia communicate utilizing these channel components to support nervous system architecture and function remain poorly understood. By studying GLR glial cells in Caenorhabditis elegans, we show that individual glial cells employ distinct innexin channel configurations to support specific functional roles, utilizing discrete downstream cellular mechanisms. We find that while innexins UNC-7and UNC-9 function as gap junction channels, the innexin INX-18 operates independently to form undocked hemichannels in discrete domains within the same cells. In this combinatorial configuration, UNC-7/UNC-9 gap junctions specifically regulate Synaptobrevin/SNB-1 localization in RME neurons, as previously reported. However, both channel types function non-redundantly to maintain glial morphology by regulating the Calpain/CLP-4 and CDK-5 pathway through cell-autonomous modulation of intracellular calcium levels. In contrast, INX-18 hemichannels in GLR glia regulate high-salt-induced paralysis behavior through distinct downstream cellular mechanisms, potentially in conjunction with tyramine signaling. Altogether, our findings demonstrate a broader repertoire of innexin channel utilization at the individual glial cell level, supporting specific aspects of nervous system maintenance and functioning.

neuroscience↗

bioRxiv2026

An Improved Protocol for High-Efficiency and Cost-Effective CRISPR/Cas9-Mediated Knock-ins in C. elegans

CRISPR/Cas9-mediated homology-directed precise genome editing using long single-stranded DNA (ssDNA) donors has expanded the possibilities for generating defined genetic modifications. However, the required ssDNA donor preparation can be technically demanding and often requires extensive locus-specific sequence design. Here, we examined parameters influencing ssDNA donor-mediated genome editing and developed approaches to simplify donor preparation using {lambda}-exonuclease-mediated ssDNA generation. By evaluating donor designs across multiple genomic loci, we found that efficient genome editing can be achieved with relatively short homology regions for a range of insertion sizes. These findings provide a basis for simplifying ssDNA donor preparation and the overall gene-editing pipeline, potentially facilitating its application across species.

molecular biology↗

bioRxiv2026

Noncoding regulatory mutations contribute to the aberrant gene expression in neuroblastoma

Comprehensive analyses of whole-genome and exome sequencing data from high-risk neuroblastoma tumors have identified relatively few recurrent and clinically actionable protein-coding driver mutations at initial diagnosis. This suggests that noncoding genetic variations that alter regulatory sequences and impact gene expression are important drivers of neuroblastoma tumorigenesis. Allele-specific expression (ASE), which quantifies differences in expression between the two alleles of a gene, is a powerful approach for identifying genes with altered dosage resulting from cis-regulatory variation. In this study, we compared ASE profiles of 156 neuroblastoma patients with 220 adrenal gland tissues from the Genotype-Tissue Expression (GTEx) Project to identify 1,363 neuroblastoma-specific ASE genes. We demonstrated that these genes were enriched for biological processes relevant to neuroblastoma pathogenesis including chromatin remodeling, protein ubiquitination, and sympathetic nervous system development, and were preferentially associated with the adrenergic transcriptional program. To elucidate the genetic mechanism underlying aberrant expression of neuroblastoma-specific ASE genes we integrated our ASE data with somatic copy number alterations (SCNA) and somatic mutation profiles. We observed that although many neuroblastoma specific ASE genes were associated with chromosomal gains and losses, a substantial subset was located within copy-number-neutral genomic regions. These genes showed significant enrichment for noncoding somatic single-nucleotide variants (SNVs) within intronic and distal intergenic neuroblastoma-specific open chromatin regions. Furthermore, functional analyses revealed that many of these SNVs disrupt transcription factor binding sites for GATA3, a core component of the regulatory circuitry that maintains the adrenergic identity of neuroblastoma cells, and neuroblastoma-specific ASE genes harboring such mutations were significantly more likely to belong to the GATA3 regulon than expected by chance. Together, our findings identify novel molecular targets of noncoding regulatory mutations in neuroblastoma and highlight the important yet underappreciated contribution of noncoding genetic variation to neuroblastoma tumorigenesis.

bioinformatics↗

bioRxiv2026

USP18-STAT2 axis enhances hepatic resilience under proteotoxic stress

The liver is a metabolic hub with a high protein turnover that renders it uniquely susceptible to proteotoxic stress. Perturbation of proteostasis, either by proteasomal inhibitors or in chronic liver diseases, could adversely impact liver physiology. Here, we show that proteasomal inhibition unexpectedly suppresses basal type I interferon (IFN-I) signaling in the murine liver. Proteasomal inhibition by bortezomib selectively downregulates a subset of interferon-stimulated genes (ISGs), among which USP18 and ISG15 emerge as critical determinants of hepatocellular survival. We identify USP18 as a central cytoprotective factor that prevents proteotoxic apoptosis independently of its deubiquitinase activity, but strictly requires its scaffolding function mediated by isoleucine-60 and interaction with STAT2. Mechanistically, proteotoxic stress disrupts IRF9 nuclear translocation, attenuating USP18 transcription, and drives USP18 and other ISGs into insoluble aggregates with kinetics distinct from canonical IFN-I-induced insolubility. Strikingly, IFN-I priming preserves ISG solubility, restores USP18 abundance, and confers resistance to proteotoxic cell death. Together, these findings uncover an unanticipated link between proteostasis and innate immune signaling, and establish the USP18-STAT2 axis to enhance hepatic resilience under proteotoxic stress.

cell biology↗

bioRxiv2026

Volatile diacetyl triggers rapid fmo-2 expression through DHAP-glycerol shunt induction

C. elegans can locate ephemeral food sources by sensing bacterially-derived volatiles. However, whether these olfactory cues can also trigger anticipatory nutrient-responsive programs remains unknown. Using unbiased transcriptomics and metabolomics, we discover that fasting worms exposed to the volatile food cue diacetyl rapidly induce expression of enzymes in the DHAP-Glycerol shunt, a metabolic pathway at the intersection of glycolysis and glycerolipid biosynthesis. We demonstrate that this pathway, known to be activated by glucotoxicity and hyperosmotic stress, is also modulated by food availability. Shunt induction requires the MDT-15 transcription factor and drives rapid metabolic remodeling, characterised by the accumulation of glycerol and phosphatidylglycerols. When food deprivation persists, the shunts activity triggers expression of the dietary restriction marker fmo-2, promoting thermotolerance and food-seeking behaviours. Our findings reveal that volatile diacetyl can rapidly modulate gene expression in C. elegans, providing new insights into the DHAP-Glycerol shunt function in metabolic homeostasis.

molecular biology↗

bioRxiv2026

Glucose-dependent regulation of hepatic adipsin controls glucose uptake and tolerance

Complement factor D, also known as adipsin, is produced by adipose tissue, and the liver that links metabolic regulation with innate immunity. Despite its established systemic functions, the regulation of hepatic adipsin expression and its contribution to metabolic disease remain poorly defined. Here, we show that hepatic adipsin protein abundance is markedly increased in individuals with type 2 diabetes (T2D), and positively correlates with glycated hemoglobin, despite unchanged mRNA expression. Concordantly, hepatic adipsin protein levels were elevated in multiple murine models of hyperglycemia, including type 1 diabetes (T1D), T2D, and following fasting-refeeding transitions. In cultured hepatocytes, glucose exposure induced a rapid, dose-dependent increase in adipsin protein without altering transcript abundance, demonstrating post-transcriptional regulation. Mechanistically, glucose stimulates adipsin translation via dephosphorylation of eukaryotic initiation factor 2 (eIF2), and activation of the mammalian target of rapamycin, mediated by the 5' untranslated region of adipsin mRNA. Functionally, hepatocyte-specific depletion of adipsin impaired postprandial glucose tolerance, with reduced glucose uptake and a marked downregulation of glucose transporter type 2 (GLUT2). Taken together, these findings identify hepatic adipsin as a glucose-responsive translational target that couples nutrient availability to metabolic adaptation, revealing a new layer of regulation with potential relevance to diabetes pathogenesis. HighlightsO_LIHepatic adipsin protein increases in type 2 diabetes and correlates with glycemic status independent of mRNA expression. C_LIO_LIGlucose induces adipsin translation through eIF2 dephosphorylation and mTOR activation. C_LIO_LImTOR controls adipsin synthesis via structured 5'UTR of adipsin mRNA. C_LIO_LILiver-specific adipsin depletion impairs post-prandial glucose tolerance by downregulating GLUT2. C_LIO_LIHepatic adipsin acts as a glucose-responsive effector of glycemic control. C_LI

cell biology↗

bioRxiv2026

Explainable AI reveals the quantitative hierarchical architecture of global bird extinction risk

Identifying what makes species vulnerable to extinction requires accounting for complex biological and environmental interactions. Due to their high predictive accuracy, machine learning methods have been widely used for these assessments; however, relying on black-box models offers limited interpretability. Here, using a comprehensive dataset of anthropogenic, ecological, morphological, demographic, and biogeographical variables from 9,053 species (81% of birds worldwide), we applied Inductive Logic Programming (ILP), an explainable artificial intelligence framework, to generate explicit and quantitative IF-THEN rules with confidence scores for bird extinction risk. Our approach revealed that extinction vulnerability follows a hierarchical structure, shaped by interactions among range size, morphological traits, and human pressures. The framework recovered well-established knowledge, while also revealing previously undescribed extinction patterns. For example, consistent with prior evidence, species with geographic ranges below [~]13,500 km{superscript 2} were identified as higher risk (88% confidence). Nevertheless, this threshold shifted to [~]3,270 km{superscript 2} when human impacts were removed, revealing quantitatively how anthropogenic activities expand the pool of vulnerable species beyond those at risk due to biological and biogeographical traits alone. Beyond established patterns, species with tail length >304 mm were identified as higher risk (82% confidence), a pattern not previously documented. ILP models achieved 91% overall accuracy, slightly lower than Random Forest (93%), but notably better than Neural Networks (83%). These results show that ILP can offer high accuracy results with full interpretability, also providing quantitative transition thresholds that clarify the structural architecture of extinction risk, and translate complex ecological interactions into actionable tools for conservation.

ecology↗

bioRxiv2026

pH Induced Changes in Protein Structure and Hydration

The molten globule (MG) state is an intermediate in the unfolding pathway of proteins, typically triggered by denaturing agents such as urea, extreme pH, high pressure, or heat. The microscopic details of such states are far from understood. Here we study the MG states in protein Hen Egg-White Lysozyme (PDB ID: 1AKI) using microscopic constant pH molecular dynamics (CpHMD) simulations and experiments across a wide pH range. We observe that the titratable residues act as key drivers of conformational fluctuations, promoting the emergence of MG states at extreme pH. These states display partial unfolding, and small global structural changes (< 7% deviation). Hydration around the fluctuating acidic residues shows reduced water density and weakened hydrogen bonding at low pH. At high pH, hydration around acidic residues increases relative to pH = 7, whereas hydration around basic residues decreases. The translational and rotational dynamics of hydration water also exhibit pronounced pH dependence: the translational diffusion coefficient (Dtrans) increases linearly with decrease in pH in acidic medium and increases linearly with increasing pH in the basic regime. The rotational diffusion (Drot) shows similar dependencies on pH except a break at pH {approx} 4 corresponding to acidic residue pKa values. Our results may be useful to identify ligand binding of lysozyme in extreme pH conditions.

biophysics↗

bioRxiv2026

Microenvironment optimization enables kidney organoid longevity with epithelial-endothelial joint basement membrane formation

Kidney organoids degrade in long-term culture and lack joint basement membranes between epithelial and endothelial cells characteristic of renal tissue. Here we show that these limitations can be overcome in static cultures simply by optimizing the microenvironment. Supplementing standard media with tubular-enhancing factors (TEFs) dramatically improves organoid yield and longevity, while vascular-enhancing factors (VEFs) and replating increases endothelial cell yield and invasiveness. A transcriptomic and imaging atlas demonstrates maintenance of nephron structures for six months with increased metabolism, signaling, differentiation, and aging-related pathways. In addition to adherent cultures, these media also enable organoid differentiation and vascularization in suspension cultures and hydrogels. Remarkably, addition of TEFs and VEFs to organoids in suspension induces self-assembly of joint basement membranes between endothelial cells and podocytes or tubules, a major feature of renal tissue. Microenvironment optimization thus enables longitudinal stabilization and higher-order vascularization of kidney organoids, offering a diverse resource for long-term studies and tissue engineering applications.

bioengineering↗

bioRxiv2026

Estradiol modulates neuronal network hyperexcitability in select NDD risk genes

Sex hormone signaling during neurodevelopment may act as a modulator of risk for neurodevelopmental disorders (NDDs), including autism spectrum disorders (ASDs). By conducting a systematic and multi-modal evaluation of estradiol effects across loss-of-function deletions in 36 functionally diverse, large-effect ASD/NDD genes in human induced pluripotent stem cell-derived neurons and larval zebrafish, we uncover convergent and divergent gene-by-estradiol interactions at the transcriptomic, circuit, and behavioral levels. Whereas estradiol partially ameliorates dysregulated expression signatures across all ASD/NDD gene knockouts examined, it selectively and rapidly dampens network hyperexcitability phenotypes in only a subset of ASD/NDD gene knockouts. Two genes, ASH1L and SCN2A, are particularly responsive to estradiol treatment, with dramatic rescue of molecular and cellular effects in human knockout neurons, coupled with behavioral phenotypes in larval zebrafish mutants. The seven most estradiol responsive genes show enhanced protein-protein interaction network connectivity, strong co-expression in specific postnatal time periods, and enrichment in upper-layer mature excitatory neurons. Altogether, we describe distinct estradiol rescue in different modalities, elucidating shared transcriptomic effects as well as gene-specific cellular and behavioral rescue in the context of loss of function mutations of select ASD/NDD genes.

genomics↗

bioRxiv2026

Direct fluorescence detection and volume electron microscopy reveal a role for antibiotic biosynthesis in the bacterial cell envelope

Secondary metabolites support the environmental fitness of a broad taxonomic diversity of bacteria and fungi, yet the cellular biology that supports secondary metabolism is little understood. This study focuses on the linearmycin antibiotics from Streptomyces sp. Mg1. These membrane-disruptive metabolites are packaged into extracellular vesicles, which in turn require the linearmycins for their biogenesis. This connection suggests that for some secondary metabolites, their biosynthesis is an integral function of cell organization and physiology. In this study, we employed simultaneous multi-photon fluorescence microscopy to directly detect linearmycins, enabling us to follow their biosynthesis and accumulation. We found that linearmycin fluorescence localizes to membrane-dense regions that also coincide with localization with a fluorescent fusion protein, LnyI-Ypet, that is essential for biosynthesis. Genetic disruption of linearmycin biosynthesis led to changes in the cell membrane visible using lipophilic dyes. To resolve differences between wild type and linearmycin-deficient membranes, we used serial FIB milling and scanning electron microscopy (FIB-SEM) to generate 3D volume reconstructions of S. Mg1 filaments. Using this approach, we identified granular subcellular compartments that require linearmycins. Disruption of linearmycin synthesis causes, in addition to disappearance of the compartments, visible distortions in the cell envelope, suggesting an integral role for the metabolites in membrane dynamics of the producer bacteria. We propose that the subcellular compartments coalesce near hyphal cell division and branch points and are regions for linearmycin biosynthesis. This study demonstrates the combined use of advanced microscopy to reveal an intrinsic role for antibiotics in the cell biology of the producing organism.

microbiology↗

bioRxiv2025

Near-atomic in-situ architecture and membrane-coupled dynamics of the Vibrio cholerae sheathed flagellum

The sheathed flagellum of Vibrio cholerae is a self-assembling membranous organelle that must coordinate axial assembly, sheath biogenesis, and rapid motor rotation. Here, we determine in-situ near-atomic structures of the sheathed flagellar motor inside intact cells. The motor anchors to the outer membrane through lipidated HL-rings without forming a membrane pore, thereby allowing axial assembly to drive sheath formation. Conserved LP-rings act as slide-rotary bushings that permit high-speed rotation within a dynamic envelope yet can constrict to seal the pore upon stress-induced ejection. We further show that stator activation requires a specific PomB-MotX interaction rather than peptidoglycan engagement. Together, these findings reveal how the distinctive architecture and dynamics of the sheathed flagellum promote V. cholerae motility, environmental survival, and persistent colonization of the human gut.

microbiology↗

bioRxiv2025

Structure of bacteriophage P1 head provides insight into capsid polymorphism

The highly regulated assembly of different proteins forming mature P1 myophage capsid show a unique polymorphism where the virion population is primarily divided in brackets of two different capsid sizes. The contrasting capsids, sized 95nm (capsid_L), triangulation number (T)=13 and 68nm (capsid_S) with T=7, both in Dextro format and have the same protein forming the phage head with similar intra and inter capsomeric interactions. Comparative study of the electron density maps of the capsids reveals the presence of protein appendages DarA and Hdf below the 5-fold symmetric region inside capsid_L that anchor the phage dsDNA to the capsid-shell. Such densities are also noticed in large capsids depleted off their dsDNA but not observed in capsid_S. Deficiency of these appendages in capsid_S results in a smaller sized dsDNA packed inside capsid_S. Despite missing out on nearly 60% of the phage dsDNA virions with capsid_S has all the essential genes responsible for the formation of a fully mature thermodynamically stable virion particle with structurally identical tail and baseplate as of capsid_L. Co-existence of both stable conformation in a single lysate is a unique phenomenon in the phage community and suggest that DarA and Hdf play an important role in phage capsid morphogenesis.

biophysics↗

bioRxiv2025

Divergence of an extracellular contractile injection system infectivity elucidated by high resolution structural studies of its tail-baseplate complex

Divergence to the infectivity practice by extracellular contractile injection systems (eCISs) is displayed by myophage P1 in its lytic phase involving its baseplate receding away from the host bacterium during infection. Atomic structure of the proteins forming P1s Tail Baseplate (TB) complex, determined here, using cryo electron microscopy are employed to identify a sequence of viral events explaining this unique phenomenon. The P1 baseplate is found to be devoid of protein appendages that are necessary for anchoring it to the host bacterium. To compensate this deficiency, P1s Long Tail Fibers (LTFs) affix to the hosts exterior, straighten up imparting stability to the virion for pursuing the infection process, thereby eliciting the baseplate hub and the tail sheath to ascend away, resulting in uniform compression of the latter. Upon the maximum unkinking of LTFs, a descending corkscrew motion commences that results in the non-uniform downward compression of the tail sheath, the tail tube and baseplate needle that perforates through the hosts membrane-cytoplasm, leading to a successful phage-bacterium infection.

biophysics↗

bioRxiv2025

Ethanolic leaf extract of Cleome spinosa induces apoptosis in Ehrlich ascites carcinoma cells through upregulation of p53 and down-regulation of Bcl-xL in vitro and in vivo

Cleome genus is commonly known as spider flower plant or cats whiskers, and is the largest genus of the family Cleomaceae, with around 200 species containing a range of remedial applications. Several species of Cleome genus show anti-cancer properties, however, nothing has been reported with genus spinosa, an anti-inflammatory and immunomodulatory plant. Thus, the present study examined the likely anti-cancer property of ethanolic leaf extract of Cleome spinosa (CSE) in Ehrlich ascites carcinoma (EAC) cells in vitro and in vivo. CSE treatment in vitro significantly caused higher percentage of death in EAC in a dose dependent manner compared to control groups (untreated and ethanol treated). Bright field, fluorescence and electron microscopies revealed apoptotic changes such as surface blebbings, nuclear fragmentation, chromatin condensation and apoptotic body formation, which probably could be the cause of death in EAC cells with CSE treatment. Apoptosis of CSE-treated EAC cells appeared to be mediated through upregulation of pro-apoptotic protein p53 and downregulation of anti-apoptotic protein, Bcl-xL expression, as ascertained through western blot both in vitro and in vivo. CSE was protective toward murine splenocytes by scavenging free radicals; it also reduced the ascitic tumor burden and increased the survival of the tumor-bearing mice compared to the control. Gas Chromatography-Mass Spectrometry (GCMS) analysis identified 43 phytocompounds in CSE. In silico molecular docking analysis indicated that a number of bioactive compounds, such as cycloartenol, stigmasterol, clionasterol, beta-sitosterol, lupenone, and sitostenone that were abundant in the CSE extract, exhibited strong binding affinities for the key apoptosis-regulating proteins, p53 and Bcl-xL. Thus, CSE derived-compounds appear to act as natural antioxidants, and have anti-cancer properties via induction of apoptosis in EAC possibly through upregulation of p53 and downregulation of Bcl-xL proteins in murine model. Hence, CSE could be considered as a promising natural compound for future cancer therapies.

cancer biology↗

bioRxiv2025

Chemical Compensation to Mechanical Loss in CellMechanosensation

Mammalian cells sense and respond to environmental changes using a complex and intelligent system that integrates chemical and mechanical signals. The transduction of mechanical cues into chemical changes modulates cell physiology, allowing a cell to adapt to its microenvironment. Understanding how the chemical and mechanical regulatory modules interact is crucial for elucidating mechanisms of mechanosensation and cellular homeostasis. In this study, we find that cells exhibit non-monotonic changes in cell volume and intracellular pH when subjected to physical stimuli and varying degrees of actomyosin cytoskeleton disruption. We discover that these non-monotonic responses are mediated by a chemical compensation mechanism, where the attenuation of actomyosin activity stimulates the activity of PI3K/Akt pathway. This, in turn, activates sodium-hydrogen exchanger 1 (NHE1), resulting in elevated intracellular pH and increased cell volume. Furthermore, we identify a competitive interaction between the PI3K/Akt and MAPK/ERK pathways - two major regulators of cell proliferation and motility. This competition modulates the chemical compensation based on the relative activities of these pathways. Our mathematical modeling reveals the network structure that is essential for establishing the non-monotonic response. Interestingly, this regulatory system is altered in HT1080 fibrosarcoma, highlighting a potential mechanistic divergence in cancer cells in contrast to their normal-like counterpart, such as NIH 3T3 and HFF-1 fibroblasts. Overall, our work reveals a compensatory mechanism between chemical and mechanical signals, providing a novel infrastructure to elucidate the integrated mechanochemical response to environmental stimuli.

biophysics↗

bioRxiv2024

Chromatin regulator HELLS mediates SSB repair and responses to DNA alkylation damage.

The SNF2 family chromatin remodeler HELLS has emerged as an important regulator of cell proliferation, genome stability, and several cancer pathways. Significant upregulation of HELLS has been reported in 33 human cancer types. While HELLS has been implicated in DNA damage response, its function in DNA repair is poorly understood. Here we report a new regulatory link between HELLS and single-strand break (SSB) repair in cellular responses to DNA alkylation damage. We found that loss of HELLS impairs SSB repair, and selectively sensitizes cells to DNA alkylating agents and PARP inhibitors (PARPi). Furthermore, we found that HELLS is co-expressed with PARP1 in cancer cells, and its loss is synthetic lethal with homologous recombination deficiency (HRD). This work unveils new functions of HELLS in modulating SSB repair and responses to clinically relevant DNA alkylation damage, thus offering new insights into the potential therapeutic value of targeting HELLS in cancer. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=158 SRC="FIGDIR/small/629292v2_ufig1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@2bbd3eorg.highwire.dtl.DTLVardef@1956f14org.highwire.dtl.DTLVardef@1afcb7corg.highwire.dtl.DTLVardef@58504c_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗