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Biology subjects

Halder, S.

Publications and source records attributed to Halder, S..

At least 19 recordsLinked to original sources

Fixation Probabilities of Mutant Alleles in an Ecological Context

For decades, population geneticists have relied upon a formula derived by Malecot and by Kimura to estimate the fixation probability of mutant alleles ({phi}). Among other things, this formula leads to the conclusion that in sufficiently large populations{phi} asymptotically approaches 2s(Ne/N ) (for small s), where s is the relative selective advantage of the mutant allele, and Ne and N respectively denote the effective and absolute (haploid) population sizes. In contrast, in sufficiently small populations,{phi} = 1/N, with the two domains of behavior being separated at the point where s [bsime] 1/(2Ne). These results hold when s, N, and Ne remain constant during the fixation process, but require modification when populations are changing in size. Here, we show that if there are ecological effects associated with competing alleles, such that the genetic composition of the population influences the total population size, the fixation probability of a beneficial allele can substantially deviate from the levels suggested above, even in the domain of effective neutrality (i.e., | s | [lsim]1/(2Ne)). We obtain analytical results for a variety of frequency-dependent functions for the overall population size, and show that the overall effect is largely a function of the response at low mutant-allele frequency. We also derive expressions for times to fixation and for fixation probabilities of deleterious alleles, and show how our results relate to prior work for the situation in which population sizes change in frequency-independent manners.

evolutionary biology↗

Renin is critical for Renin Lineage Cell Plasticity and Migration in experimental crescentic Glomerulonephritis

Key PointsO_LIRenin deficiency in renin-lineage cells worsened crescentic injury and impaired cell migration, revealing a protective role for renin in crescentic glomerulonephritis. C_LIO_LILoss of renin shifted renin-lineage cells signaling toward interferon/STAT1-driven C_LIO_LIRenin-lineage cell ablation in crescentic glomerulonephritis induced a less inflammatory disease time-course. C_LI BackgroundThe adult juxtaglomerular renin-lineage cell (RLC) niche contributes to intraglomerular repair after injury, but their role in highly inflammatory crescentic glomerulonephritis (cGN) remains unclear. While angiotensin II-AT1R signaling promotes fibrosis and inflammation, the contribution of the RLCs, and of renin expression within RLCs, to cGN outcome has not been investigated. MethodsWe used tdTomato lineage-tracing to track RLCs in wild-type (WT) and renin-knockout (RenKO) mice following cGN induction. RLC migration and glomerular injury were quantified histologically. Single-cell RNA sequencing was performed on isolated tdTomato-positive cells at day 10 and 21 after injury to characterize transcriptional programs. Disease progression was additionally examined in mice with diphtheria toxin A-mediated (DTA) RLC ablation. ResultsRLCs were detected within injured glomeruli during cGN, with sporadic localization to crescentic lesions. Genetic renin deletion in RLCs worsened cGN outcomes, with RenKO mice developing increased albuminuria (by 306%), crescent formation (by 50%) and podocyte loss (by 15%) by day 21 compared to WT controls. Renin-deficient RLCs exhibited a reduced intraglomerular migratory response with decreased colocalization with mesangial and podocytes cell markers. Single-cell transcriptomic analysis supports an immunomodulatory reparative phenotype in WT RLCs. In contrast, RenKO RLCs displayed enrichment of interferon-stimulated genes and pathways suppressing cell migration. RLC ablation reduced macrophage infiltration, but did not alter disease progression, suggesting compensatory cellular mechanisms. ConclusionsRenin expression supports the plasticity and injury-associated responses of RLCs during cGN. Loss of renin shifts RLCs toward an interferon-driven inflammatory and antimigratory phenotype that aggravates glomerular injury, while ablation of the RLCs may be compensated without major outcome changes.

pathology↗

Topological Entropy Correlates with the Predictive Power of Multiplexed Ensemble Reservoir Computing

Modeling nonlinear, multiscale, and transiently chaotic biological processes remains a major challenge in computational biology. Traditional deep learning models, while powerful, require large datasets and lack mechanistic interpretability, limiting their effectiveness for time-resolved biological systems. Reservoir computing (RC) offers a promising alternative by leveraging the rich transient dynamics of fixed nonlinear systems, yet standard RC architectures struggle with high-dimensional biological data and complex temporal regimes. Here, we introduce Dynamical System Machine Learning (DynML), a multiplexed reservoir framework designed to model gene-expression dynamics in systems such as liver regeneration and Drosophila embryogenesis. DynML encodes biological signals using heterogeneous Lorenz reservoirs and employs a single global readout to capture stage-dependent dynamics with high predictive accuracy. We further show that reservoir topological entropy quantitatively predicts model performance, linking dynamical richness to biological forecasting accuracy. Beyond biological time-series modeling, we demonstrate the generality of DynML on the MNIST handwritten digit classification task using a Rossler-based chaotic reservoir, showing that fixed dynamical cores with linear readouts can also support high-dimensional static classification. Overall, DynML provides a scalable, interpretable, and computationally efficient framework that unifies biological time-series modeling and conventional machine-learning tasks within a single dynamical systems paradigm. Author summaryComplex biological phenomena such as development, regeneration, and disease progression emerge from time-dependent gene-expression programs governed by nonlinear, multiscale dynamics. Capturing these dynamics remains challenging for conventional machine-learning approaches, which typically require large datasets and lack interpretability. In this study, we introduce Dynamical System Machine Learning (DynML), a modeling framework that leverages the transient dynamics of chaotic systems to learn and predict biological time series. DynML transforms gene-expression measurements into high-dimensional dynamical representations using ensembles of nonlinear reservoirs, enabling accurate prediction of future expression states with simple and interpretable linear readouts. We apply DynML to both synthetic dynamical systems and real biological datasets, including Drosophila embryonic development and human liver regeneration, where it achieves high predictive accuracy across multiple temporal transitions. Importantly, we show that the predictive performance of DynML is strongly linked to the topological entropy of the reservoir dynamics, providing a principled and quantitative measure of model expressiveness. Beyond biological time-series prediction, we demonstrate that the same dynamical framework can also classify static data, achieving strong performance on handwritten digit recognition. Together, our results establish DynML as a scalable and interpretable approach for modeling complex biological dynamics, and highlight how concepts from dynamical systems theory can guide the design of effective machine-learning models for biological data.

systems biology↗

Mon1-Rab7 axis is essential for transport, localization and anchoring of oskar mRNA

Asymmetric localization of oskar mRNA to the posterior of the oocyte is a complex process driven by autonomous and non-cell autonomous mechanisms. The former includes Oskar protein that reinforces localization and anchoring of its mRNA through activation of endocytosis and regulation of actin cytoskeleton; the latter includes signals from the posterior follicle cells (PFCs) that regulates microtubule orientation for polarized transport. Here we identify Monensin Sensitivity 1 (Mon1), as a novel factor regulating anterior-posterior (A-P) patterning. Mon1 is an evolutionarily conserved activator of Rab7-a key regulator of the endo-lysosomal pathway. Embryos lacking maternal mon1 (mon1m) show mislocalized oskar and bicoid mRNAs leading to loss of patterning and lethality. In the mutant oocyte Staufen appears clumpy and the levels of Oskar protein and Par-1 is significantly reduced. Abnormal actin rings are seen in the ooplasm. Driving expression of mon1 in the germline rescues these phenotypes and restores viability. In contrast, expression in the PFC predominantly rescues the Par-1 phenotype with a modest effect on viability. We demonstrate that oskar mRNA interacts with Rab7 suggesting possible role for the Mon1-Rab7 axis in the transport of oskar. We show that Mon1 in the PFCs, regulates PIP2 levels to influence accumulation of Par-1 in the oocyte. We propose that Mon1 regulates oskar localization in two distinct ways: cell autonomously in the germline by regulating Rab7, and non-cell autonomously through the PFCs by regulating accumulation of Par-1. Summary statementMon1, an established Rab converter, has roles in embryonic axial patterning, modulating transport, localisation and anchoring of posteriorly localised mRNA during oocyte maturation. Mon1 influence is both cell autonomous, from within the oocyte and non-cell autonomous, through posterior follicle cells.

developmental biology↗

A transcription factor-responsive enhancer discovery platform for targeted immunotherapy

Synthetic enhancers with high specificity are crucial for therapeutic gene control. However, experimental screens and machine learning-guided design typically require context-specific datasets, limiting generalizability. Because transcription factor (TF) activity reflects cellular state, TF-responsive enhancer libraries offer a universal starting point. Here, we developed TREND (transcription factor-responsive enhancer discovery), a massively parallel reporter assay of [~]2.7 million enhancer-barcode constructs representing 57,715 designs. TREND covers 1,068 motif-annotated proteins, including 729 confirmed TFs across 49 DNA-binding domain families. Applied to ovarian cancer, TREND identified enhancers that discriminate cancer from normal epithelial cells. These enhancers enabled protein-interaction-based AND-gate circuits with reduced OFF-state leakage and amplified ON-state output, driving tumor-restricted expression of combinatorial immune effectors and robust antitumor responses in murine ovarian cancer models. TREND also identified T-cell activation-responsive enhancers with greater inducibility and lower basal activity than conventional NFAT-motif-based elements. Together, TREND provides a generalizable framework for context-specific enhancer discovery and therapeutic gene regulation.

synthetic biology↗

Metabolic plasticity drives mechanisms of PARP inhibitor persistence in ovarian cancer

PARP inhibitors (PARPi) are the standard maintenance therapy for ovarian cancer, but the frequent emergence of resistance remains a major clinical challenge. Emerging evidence suggests that tumor cell plasticity is an important mechanism enabling this adaptive resistance. In this study, we combined both experimental and computational techniques to model this evolutionary process by long term treatment of the OVCAR3 ovarian cancer cell line with Olaparib (a PARPi). We then performed single-cell RNA sequencing (scRNAseq) on both naive and persistent cells to capture cancer cells heterogenous response. scRNAseq profiling suggested an adaptive metabolic reprogramming in response to long term Olaparib treatment. We then scored single cells for metabolic function, and persister cells were found to have reprogrammed their glutamine metabolism. To test these findings, both persister and naive cells were cultured in glutamine-deprived media and persister cells were found to have higher viability than the naive cells particularly when exposed to Olaparib. To test the cells capacity to switch their metabolic state toward glycolysis, we performed Seahorse mitochondrial and glycolytic stress tests. These analyses revealed that persister cells were less dependent on glutamine metabolism and instead exhibited increased glycolytic capacity compared to naive cells. This metabolic shift resulted in an acquired dependency on glucose, representing a potential therapeutic vulnerability. Together, these results indicate that prolonged Olaparib exposure promotes metabolic plasticity in ovarian cancer cells. To explore how this plasticity might be exploited therapeutically, we developed a proof-of-concept mathematical model that leverages metabolic state transitions to optimize treatment scheduling. ONE SENTENCE SUMMARYOvarian cancer cells exploit metabolic plasticity to increase their evolvability to persist PARP inhibitor treatment.

cancer biology↗

Live-cell imaging and lipidomics of low density lipoprotein containing intrinsically fluorescent cholesteryl esters

Low density lipoprotein (LDL) delivers cholesterol to cells in the body in the form of cholesteryl esters (CEs), and dysfunction of this pathway is associated with various diseases. Due to the lack of suitable tools, our understanding of the intracellular transport and hydrolysis of CEs is limited. We present a novel approach for studying LDL-derived CEs in cells, using fatty acyl chain conjugates of the intrinsically fluorescent cholestatrienol (CTL). We demonstrate that CTL esters reconstituted into LDL particles are hydrolyzed in late endosomes and lysosomes (LE/LYSs) by acid lipase, while an LDL-derived CTL ether analog cannot leave LE/LYSs. Using live-cell imaging, lipidomics, and multimodal Bayesian modeling, we discover a sequential biphasic transport of LDL-derived CTL to LE/LYSs matching the kinetics of the lysosomal hydrolysis of LDL-associated CTL-ester with a half-time of 3.0 hours. Hydrolyzed CTL derived from LDL-associated CTL esters is rapidly re-esterified with a similar half-time and stored in lipid droplets, demonstrating efficient sterol transport to the endoplasmic reticulum (ER). The latter is supported by the detection of a faint CTL staining in the ER and by extensive contact formation between endo-lysosomes containing LDL and ER tubules. Using lipidomics and Bayesian kinetic modeling, we also track LDL-derived CEs and triacylglycerols in cells and determine the uptake kinetics for each lipid species individually. Our novel approach allows for precise measurement of post-endocytic trafficking and metabolism of LDL-derived cholesterol and other lipids in living cells.

biochemistry↗

IFI16 senses and protects stalled replication forks

Replication stress is a key driver of DNA damage and genome instability. Replication stress-induced fork remodelling generates a new DNA end that is vulnerable to the action of nucleases, and which is protected by a range of factors including the canonical tumour suppressors BRCA1 and BRCA2. Here we report that replication stress drives elevated production of cytokines and chemokines in the absence of DNA damage. The DNA sensor IFI16 binds nascent DNA at stalled replication forks and signals via the DNA sensing adaptor STING, to induce the activation of NF-{kappa}B and the production of pro-inflammatory cytokines in response to replication stress. IFI16 also acts directly at stalled replication forks to protect nascent DNA from degradation by the nucleases MRE11 and DNA2. Furthermore, IFI16 is required for the interferon-mediated rescue of fork protection in BRCA-deficient cells, highlighting the critical role of IFI16 in the cross-talk between innate immunity and fork protection during replication stress. HighlightsO_LIReplication stress induces an early innate immune response, which is dependent on the DNA sensing factors IFI16 and STING, but not cGAS C_LIO_LIIFI16 binds directly to nascent DNA at stalled replication forks C_LIO_LIIFI16 prevents nucleolytic degradation of reversed forks C_LIO_LIIFI16 is required for interferon-mediated fork protection in BRCA-deficient cells C_LI

cancer biology↗

Donor-Specific Digital Twin for Living Donor Liver Transplant Recovery

Liver resection initiates a meticulously coordinated hyperplasia process characterized by regulated cell proliferation that drives liver regeneration. This process concludes with the complete restoration of liver mass, showcasing the precision and robustness of this homeostasis. The remarkable capacity of the liver to regenerate rapidly into a fully functional organ has been crucial to the success of living donor liver transplantation (LDLT). In healthy livers, hepatocytes typically remain in a quiescent state (G0). However, following partial hepatectomy, these cells transition to the G1 phase to re-enter the cell cycle. Surgical resection induces various stresses, including physical injury, altered blood flow, and increased metabolic demands. These all trigger the activation and suppression of numerous genes involved in tissue repair, regeneration, and functional recovery. Both coding and noncoding RNAs detectable in the bloodstream during this process provide valuable insights into the gene responses driving liver recovery. This study integrates clinical gene expression data into a previously developed mathematical model of liver regeneration, which tracks transitions among quiescent, primed, and proliferating hepatocytes to construct virtual, patient-specific liver models. Using whole transcriptome RNA sequencing data from 12 healthy LDLT donors, collected at 14 time points over a year, we identified liver resection-specific gene expression patterns through Weighted Gene Co-expression Network Analysis (WGCNA). These patterns were organized into distinct clusters with unique transcriptional dynamics and mapped to model variables using deep learning techniques. Consequently, we developed a Personalized Progressive Mechanistic Digital Twin (PePMDT) for the livers of LDLT donors. The resulting PePMDT predicts individual patient recovery trajectories by leveraging blood-derived gene expression data to simulate regenerative responses. By transforming gene expression profiles into dynamic model variables, this approach bridges clinical data and mathematical modeling, providing a robust platform for personalized medicine. This study highlights the transformative potential of data-driven frameworks like PePMDT in advancing precision medicine and optimizing recovery outcomes for LDLT donors.

systems biology↗

Expansion of Drosophila haemocytes using a conditional GeneSwitch driver affects larval haemocyte function, but does not modulate adult lifespan or survival from infection

Macrophages are responsible for diverse and fundamental functions in vertebrates. Fruit flies harbour an innate immune system of which the most populous blood cell (haemocyte) type bears striking homology to the vertebrate macrophage. The importance of these cells has been demonstrated previously, where immune and developmental phenotypes have been observed upon haemocyte ablation using pro-apoptotic transgenes driven by the Hml promoter. Here we show that, as well as ablating Hml-positive cells in vivo using the pro-apoptotic transgene bax, we can also increase Hml-positive cell numbers using a constitutively-active form of ras. However, in adults, compared to larvae, total blood cell numbers were not significantly affected by experimental expansion or ablation. This therefore implies the existence of feedback mechanisms which regulate the number of haemocytes. No effect on lifespan was observed from driving ras and bax in Hml-positive cells using a conditional genetic system (Hml-GeneSwitch). Using a constitutive driver system, we did observe differences in lifespan, however we attribute this to differences in genetic background that could have led to spurious conclusions. Additionally, no effect of either transgene was observed upon infection with two different bacterial species, although a striking pupal lethality phenotype was observed upon expansion of Hml-positive cells in the context of a self-encapsulation mutant genetic background. The latter confirms that the change in Hml-positive cell number does result in a phenotype. The lack of adult phenotypes could be due to the strength of our experimental manipulation or due to compensation via feedback mechanisms that operate to maintain total blood cell numbers. Our study demonstrates the importance of a conditional approach to modulate haemocyte cell numbers in vivo which allows for more precise study of innate immune system function. This approach could be especially fruitful to uncover the mechanisms that regulate total blood cell numbers across development and ageing.

developmental biology↗

Nutrition and density dependence of spontaneous female-biased dispersal in Drosophila

Dispersal is often essential for the attainment of Darwinian fitness, especially for species living on spatially structured, heterogeneous habitats. Theoretically, sex-specific resource requirement can drive the two sexes to disperse differently, resulting in sex biased dispersal (SBD). Understanding ecological factors affecting SBD is important. Using an experimental two-patch dispersal setup we measured spontaneous dispersal in laboratory adapted populations of Drosophila melanogaster under a set of common, interlinked ecological scenarios relating to - (a) dietary ecology and (b) adult density. We found deteriorating overall nutritional quality of food affects strength of SBD, and female dispersal is particularly sensitive to availability of protein. Adult density had sex specific effect on dispersal. Female dispersal was found to be density independent but males showed increased dispersal at higher density. Female tend to disperse more from male biased patch likely to avoid male harassment whereas absence of female drives male dispersal solidifying mate-finding dispersal hypothesis. These evidences of dispersal suggest that variation in dietary ecology and intraspecific competition can affect the degree and strength of existing SBD and thereby male-female interactions in a patch potentially affecting fitness components and population dynamics.

evolutionary biology↗

Gynura procumbens Leaf Extract-Loaded Self-Microemulsifying Drug Delivery System Offers Enhanced Protective Effects in the Hepatorenal Organs of the Experimental Rats

Gynura procumbens, known as longevity spinach, is a plant traditionally used in tropical Asian countries for its anti-inflammatory, hepatoprotective, anti-hypertensive, anti-hyperglycemic, and anti-inflammatory properties. The current study aimed to enhance the hepatorenal protective activity of Gynura procumbens leaf extract (GLE) by developing a self-microemulsifying drug delivery system (SMEDDS). SMEDDS-GLE exhibited the formation of small micelles with a mean droplet size of 231 nm. This resulted in a significant enhancement in the dispersion of GLE in water, as evidenced by a dispersibility that was at least 4.8 times greater than that of GLE alone. In the rat model of hepatic injury induced by cisplatin (7.5 mg/kg, i.p.), the administration of SMEDDS-GLE (75 mg-GLE/kg, p.o.) significantly reduced liver damage, observed by histological examination and reduced levels of plasma biomarkers associated with hepatic injury. Furthermore, according to histological examination findings and plasma biomarkers assessment, SMEDDS-GLE enhanced nephroprotective benefits of GLE in the rat model of acute kidney injury. Based on these findings, a strategic application of the SMEDDS-based approach could be a viable choice to enhance GLEs nutraceutical properties.

pharmacology and toxicology↗

Distinct neural bases of subcomponents of the attentional blink

The attentional blink reflects a ubiquitous bottleneck with selecting and processing the second of two targets that occur in close temporal proximity. An extensive literature has examined the attention blink as a unitary phenomenon. As a result, which specific component of attention - perceptual sensitivity, choice bias or both - are compromised during the attentional blink, and their respective neural bases, remains unknown. Here, we address this question with a multialternative task and novel signal detection model, which decouples sensitivity from bias effects. We find that the attentional blink impairs specifically one component of attention - sensitivity - while leaving the other component - bias - unaffected. Distinct neural markers of the attentional blink mapped on to distinct subcomponents of the sensitivity deficits. Parieto- occipital N2p and P3 potential amplitudes characterized target detection deficits whereas long- range high-beta band (20-30 Hz) coherence between frontoparietal electrodes signalled target discrimination deficits. We synthesized these results with representational geometry analysis. The analysis revealed that detection and discrimination deficits were encoded along separable neural dimensions, whose configural distances robustly correlated with the neural markers of each. Overall, these findings provide detailed insights into the subcomponents of the attentional blink, and reveal dissociable neural bases underlying its detection and discrimination bottlenecks. Lay summaryIn daily life, our attention switches rapidly between different objects. For example, when driving, we may shift focus from a billboard on the roadside to a pedestrian in front, in quick succession. Yet, our ability to process the second object is severely compromised especially when it appears soon after the first: an impairment called the "attentional blink". In previous work, the attentional blink has been studied essentially as a "monolithic" (indivisible) phenomenon. We design a behavioral model to divide the attentional blink into sub- components and show that the blink affects only one specific component (sensitivity). We also identify key neural markers for deficits associated with this component. Our findings may aid in understanding the neural origins of attention deficit disorders.

neuroscience↗

Synthesis and characterization of novel intrinsically fluorescent analogs of cholesterol with improved photophysical properties.

Live-cell imaging of cholesterol trafficking depends on suitable cholesterol analogs. However, existing fluorescent analogs of cholesterol either show very different physico-chemical properties compared to cholesterol or demand excitation in the ultraviolet spectral region. We present novel intrinsically fluorescent sterols containing four conjugated double bonds in the ring system and either a hydroxy or a keto group in the C3 position. Synthesis of these probes involves dehydrogenation of 7-dehydrocholesterol using mercury(II) acetate, Swern oxidation/dehydrogenation, and stereoselective Luche reduction. Molecular dynamics simulations and nuclear magnetic resonance spectroscopy reveal that the analog with a 3-hydroxy-group like cholesterol can condense fatty acyl chains and form hydrogen bonds to water molecules at the bilayer interface. The emission of both probes is red-shifted by 80-120 nm compared to the widely used sterol analogs dehydroergosterol or cholestatrienol. This allows for their imaging on conventional microscopes, as we here show in giant unilamellar vesicles. These experiments reveal a preferred partitioning of both sterol probes into the biologically relevant liquid-ordered phase. In conclusion, we present a synthesis strategy leading to novel intrinsically fluorescent sterol probes with close resemblance of cholesterol. Their improved photophysical properties will allow for live-cell imaging of sterol transport in the future.

biophysics↗

Ecdysone Orchestrates Notch and Broad Symphony to Craft Epithelial Cell Shape Change

Morphogenesis in the metazoans relies on cell shape transformations that forms an integral component of organ development, form generation and maintenance of tissue homeostasis. Nevertheless, a comprehensive grasp of how the epithelial morphogenesis is modulated in the metazoans remain still elusive. The Steroid hormones play a pivotal role in morphogenesis spanning several organs including the gonads, urogenital tracts, and mammary glands. Employing the Drosophila oogenesis model, we investigated the the role of steroid hormone receptor, Ecdysone receptor (EcR) involvement in transforming anterior epithelial follicle cells (AFCs) from cuboidal to squamous shape. Consistent with the fact that the activity of EcR in the AFCs coincides with the timing of cuboidal-to-squamous shape transition, we found that depletion of EcR function impedes the shape transformation of AFCs. We report that EcR doesnt impair the follicle cell fate, but impedes the morphological change by restricting the remodelling of lateral and adherens junctions. Employing the classical genetic tools and immnohistochemistry, we show that EcR limits the Notch-Broad axis to facilitate alteration of the shape of AFCs. Our study suggests a mechanistic model where Ecdysone signalling, via the Notch pathway, finetunes the activity of non-muscle myosin heavy chain zipper, prompting AFC shape transition. In sum, our work illuminates how Ecdysone signalling orchestrates epithelial follicle cell morphogenesis during metazoan development.

developmental biology↗

TOR signalling regulates epithelial cell shape transition in Drosophila oogenesis

Epithelial morphogenesis plays an important role in form generation, organ development, and maintenance of adult tissues in the metazoans. Given its wide implication, aberrant morphogenesis is linked to severe developmental defects and in a few instances also associated with tumorigenesis. Employing the model of Drosophila oogenesis, we have examined the role of the evolutionary conserved Target of Rapamycin (TOR) kinase pathway, a known regulator of cell growth and size in mediating shape transition of cuboidal cells to squamous epithelial fate. Utilizing genetic tools, immunohistochemistry, and live cell imaging, we demonstrate that TOR signaling is active and required for epithelial morphogenesis during Drosophila oogenesis. Further, loss of function analyses indicates that non-canonical TOR signaling functions through PAR-1 to mediate the removal of lateral cell adhesion molecule, Fasciclin 2, to allow proper squamous cell morphogenesis. In addition, we demonstrate the effect of TOR through PAR-1 on cell shape transition is mediated via the modulation of endocytosis. Overall, our data give novel insight into how TOR signaling mediates cell shape transition during epithelial morphogenesis in the metazoans.

developmental biology↗

Spatial structure does not reduce population level interlocus sexual conflict but imposes additional sex-specific costs

Spatial structure is a common feature of all naturally occurring populations. Theoretically, spatial structuring of a habitat could modulate the intensity of Interlocus sexual conflict (ISC) in a population, possibly by modulating intersexual encounter rate. We tested this theory using laboratory populations of Drosophila melanogaster by measuring male induced fitness decline in females in three-patch habitat systems under two alternative habitat types - structured-interconnected and unstructured. Our results on reproductive and survival costs in females suggested significant costs due to (a) male presence (i.e., ISC) and (b) living on structured habitat. However, there was only a weak evidence supporting the theory of modulation of ISC by habitat structuring only. Through a follow up experiment, we further showed that the effect of habitat on ISC is also robust to the alteration of female conditions. Therefore, it appears that spatial structuring per se is unlikely to modulate ISC, but can impose additional survival costs. We further showed such survival cost could be sex-specific possibly reflecting female biased spontaneous dispersal.

evolutionary biology↗

Removal Of Environmental Pollutants (Lead, Chromium And Cadmium) Using Root And Leaf Tissues Of Indian Mustard, Rice And Wheat Plants

The environment is polluted day by day and it is very much expensive to remediate the environmental pollutants by physicochemical process. Therefore, using plants as a process to remediate pollutants is essential. In this study, phytoremediation of root and leaf tissues of Indian mustard (Brassica juncea), rice (Oryza sativa) and wheat (Triticum aestivum) against three most environment pollutants viz. lead (Pb), chromium (Cr) and cadmium (Cd) of Buriganga riverbank soil of Dhaka city, Bangladesh were assessed. The highest amount of Pb was found in the leaf (11.6755 {+/-}1.9860 mg/kg dry weight) and root (51.4251 {+/-}5.0320 mg/kg dry weight) of B. juncea. However, the highest amount of Cr was found in the leaf (5.9871{+/-}0.9032 mg/kg dry weight) of B. juncea; and in the root (46.4739{+/-}2.2920 mg/kg dry weight) of O. sativa respectively. Although the highest amount (0.9624{+/-}0.0920 mg/kg dry weight) of Cd was found in the leaf of B. juncea; the amount of Cd in the root was approximately same in all the three plants. This research also found more amounts of heavy metals compared to other studies using Indian mustard, rice and wheat against the three most environmental pollutants viz., Pb, Cr and Cd. Moreover, this study revealed that B. juncea is the highest hyperaccumulator species regarding Pb, Cr and Cd accumulation and can be used to clean up the polluted Buriganga riverbank soil.

plant biology↗