Biology subjects

Fatima, S.

Publications and source records attributed to Fatima, S..

13 recordsLinked to original sources

bioRxiv2026

Prime Editing Corrects the HBB Codon 8/9 (+G) Mutation in Patient-Derived Induced Pluripotent Stem Cells and Restores β-Globin Expression in iPSC-Derived Erythroid Cells

Homozygosity for the HBB codon 8/9 (+G) frameshift (c.27dup (p.Ser10ValfsTer14)) causes transfusion-dependent {beta}-thalassaemia and is common in South Asia. Prime editing can reverse this insertion without double-strand breaks or donor DNA, but its efficiency depends on pegRNA design. We derived Sendai-reprogrammed iPSCs from a homozygous patient, optimised PEmax editing (spacer, pegRNA extension, secondary nick, MLH1dn) and compared patient, PEmax-treated and control iPSC-derived erythroid cells by flow cytometry, colony assays, RT-qPCR, western blotting and cation-exchange HPLC. Patient iPSCs had a normal 46,XY karyotype, expressed pluripotency markers, formed all three germ layers and were Sendai-free by passage 15. A PAM-disrupting spacer with a +68 nicking sgRNA gave the highest intended-edit frequency 8.4%; MLH1dn added little. PEmax-treated cultures matured and formed colonies more like control than patient cultures, restored HBB transcript (about 4-fold control iPSC-derived cells) and detectable {beta}-globin protein, and contained an HPLC fraction consistent with HbA ( undetectable in patient cells). Fetal haemoglobin (about 80%) and embryonic globin remained predominant. Prime editing corrects HBB c.27dupG in patient iPSCs and restores {beta}-globin expression, with partial restoration of adult haemoglobin in a fetal/embryonic-type erythroid background. Validation in additional donors, haematopoietic stem cells and in vivo is required.

cell biology↗

bioRxiv2026

Genome-wide analysis reveals the importance of histone acetyltransferase Esa1 in transcriptional regulation during nitrogen starvation

Macroautophagy/autophagy is a process that degrades intracellular components and is strongly triggered by nitrogen starvation (-N). Some ATG (autophagy related) genes are activated at the transcriptional level in nitrogen starvation; however, a full understanding of transcriptional induction and the role of chromatin during this process remains unclear. To address this, we measured the occupancy of RNA polymerase II (Pol II), histone H3, and acetylated H4 (H4Ac) under nutrient-rich and -N conditions by ChIP-seq. We found that most genes are rapidly downregulated within 15-30 min, including ribosomal protein (RP) and biogenesis (RiBi) genes. Meanwhile, genes involved in amino acid (AA) biosynthesis are upregulated, along with many ATG genes. Unexpectedly, RP and RiBi genes were reinduced by 3 hours. Furthermore, many upregulated genes remained active during prolonged starvation. Histones are typically removed from promoters during transcription activation. Consistent with this, we found that most induced genes exhibited histone eviction and increased H4 acetylation at their promoters, suggesting a possible role for histone acetylation in their activation. In line with this, depleting Esa1, an essential H4 histone acetyltransferase, nearly abolished the induction of ribosomal biosynthetic genes and many AA biosynthetic genes. Sustained activation of many genes during prolonged starvation highlights the vital role of transcription in supporting autophagy and cell survival. This is the first comprehensive study to detail changes in chromatin, histone acetylation, and transcription during nitrogen starvation, highlighting the importance of Esa1 and H4Ac in this process.

genetics↗

bioRxiv2026

Does Low Dose Radiation Induced Adaptive Response Influence Initial DNA-DSB formation? Evidence from γH2AX foci Analysis in Human Lymphocytes

PurposeLow-dose radiation-induced adaptive response (LDRIAR) is well documented, but its role in early DNA damage signalling remains unclear. This study aimed to investigate whether adaptive response influences initial DNA double-strand break (DSB) recognition, as reflected by {gamma}H2AX foci formation, and to evaluate its time-dependent expression in human lymphocytes. Materials and MethodsPeripheral blood lymphocytes from three healthy donors were exposed to a priming dose followed by a challenging dose at defined time intervals. DNA damage was assessed using {gamma}H2AX foci analysis, comparing acute and split-dose exposures in both PHA-stimulated (large) and non-stimulated (small) lymphocytes. ResultsA clear time-dependent adaptive response was observed. No significant reduction in {gamma}H2AX foci was detected at 1 h (p > 0.05). At 2 h, a significant decrease was observed ([~]7-8% in large and [~]13% in small lymphocytes; p < 0.01), which increased at 4 h ([~]12% and [~]22%, respectively; p < 0.001). The maximal response occurred at 15 h, with reductions of [~]40- 43% in large and [~]27% in small lymphocytes (p < 0.001). Small lymphocytes exhibited an earlier response, while large lymphocytes showed a greater magnitude at later time points. The temporal trend was consistent across donors, with minor variability at later intervals. ConclusionsThe findings demonstrate that LDRIAR is reflected at the level of DNA damage signalling and follows a defined temporal pattern with cell-type specificity. This suggests that adaptive response may influence early DSB-associated processes, contributing to a better understanding of radiation response mechanisms in radiobiology.

molecular biology↗

bioRxiv2026

NR4A1 limits CD8⁺ T Cell effector responses and protection in tuberculosis

During Mycobacterium tuberculosis (Mtb) infection, CD8+ T cells exhibit dysfunction with impaired cytotoxicity and limited localization to granuloma cores. Using knockout mice, adoptive-transfer models and validation in macaque and human datasets, we identified the nuclear receptor NR4A1 as a key restrainer of CD8+ T cell immunity in tuberculosis (TB). Mtb-infected Nr4a1-/- mice displayed reduced bacterial burden, attenuated pathology, higher lung CD8+/CD4+ T cell ratios, and enhanced CD8+ T cell effector functions. Bulk and single-cell RNA sequencing revealed suppression of gene expression program linked with exhaustion, and expansion of Nkg7+ and Granzyme+ cytotoxic CD8+ T cell subsets in Nr4a1-/- mice. Spatial analyses demonstrated increased infiltration of Nkg7+ activated CD8+ T cells in Nr4a1-/- lesions. ChIP-qPCR showed NR4A1 binding to Nkg7 promoter, and Nkg7 knockdown abrogated the enhanced cytotoxicity of Nr4a1-/- CD8+ T cells. Pharmacologic inhibition of NR4A1 reduced Mtb burden and pathology, and restored Nkg7 expression and CD8+ T cell infiltration in the lung. Together, these findings identify NR4A1 as a negative regulator of CD8+ T cell-mediated immunity in TB and suggest the NR4A1-NKG7 axis as a novel host-directed therapeutic target. A one-sentence summary of your paperNR4A1 suppresses CD8+ T cell infiltration and cytotoxicity in TB lesions, and its inhibition enhances host resistance to Mtb infection.

immunology↗

bioRxiv2024

TGF-β expressed by M2 macrophages promotes wound healing by inhibiting TSG-6 expression by mesenchymal stem cells

Wound healing involves the collaboration of multiple cells, including macrophages and fibroblasts, and requires the coordination of cytokines, growth factors, and matrix proteins to regulate the repair response. In this study, we investigated how M2 macrophages regulate expression of the anti-fibrotic and anti-inflammatory regulator tumor necrosis factor- (TNF-)-stimulated gene 6 (TSG-6) secreted by adipose tissue-derived stem cells (ASCs) during wound healing. Interleukin (IL)-4/IL-13, which is used to differentiate macrophage M2 phenotypes, increases TSG-6 in ASCs; however, M2 macrophages significantly decrease TSG-6 in ASCs. Transforming growth factor (TGF)-{beta} expression was increased, and TNF- expression was decreased in M2 macrophages. TGF-{beta} inhibited IL-4/IL-13-induced ASC TSG-6 expression. In addition, TSG-6 suppressed TGF-{beta}-triggered wound closure and fibrogenic responses in LX-2 cells. Collectively, TSG-6 inhibited wound healing, but M2 macrophage-expressed TGF-{beta} prevented TSG-6 production from ASCs, which ultimately helped wound healing. Our results indicate that the balance of TNF- and TGF-{beta} levels during wound healing regulates TSG-6 production from ASCs, which may ultimately modulate the healing process. Our study findings could contribute to novel therapeutic strategies that manipulate the delicate balance between TNF- and TGF-{beta} to enhance wound repair and mitigate fibrosis.

cell biology↗

bioRxiv2024

A Rapid, Cost-Effective Method for High-Yield DNA Purification from PCR Products and Agarose Gels.

Nucleic acid purification is essential for molecular biology workflows, enabling successful downstream applications like cloning, sequencing, and PCR amplification. While commercial kits are widely used for DNA extraction from PCR products and agarose gels, their high costs can burden resource-limited laboratories. To provide a viable alternative, we developed an optimized, cost-effective in-house protocol for high-yield DNA purification. This study evaluates the performance of our protocol for plasmid DNA and PCR products, comparing it with commercial kits from Qiagen, Thermo Fisher, and WizBio in terms of cost, time, DNA concentration, and purity. Results from gel electrophoresis demonstrated that the in-house protocol significantly enhances PCR product clarity and reduces background smearing, yielding high-purity DNA compatible with sensitive applications. Restriction-digested plasmid samples showed successful ligation and transformation in E. coli (DH5), with Sanger sequencing chromatogram further confirming the sequence integrity of the purified DNA. Our findings highlight the in-house protocol as a cost-effective, efficient, and reliable alternative to commercial kits, delivering high-quality DNA suitable for various molecular applications. This method offers an accessible and practical solution for laboratories seeking to optimize DNA purification under budget constraints.

molecular biology↗

bioRxiv2023

Genetic Association of PLAG1 Gene Variant 14:25015640G>T with Wither-Height in Pakistani Cattle

The cow is one of the most valuable domesticated animals, producing milk, meat, fiber, hide and manure for agricultural purposes to serve humanity. Particularly, first two production traits are significantly linked with the physical characteristics of the animal e.g., wither-height, large body-size and skeletal frame are positively correlated with these production traits. The PLAG1 is one of the many genes that has been associated with the aforementioned trait in many livestock and human species. So, the current study was conducted on a total of 50 cattles using ARMS-PCR genotyping technique followed by genetic association testing of the 14:25015640G>T variant using PLINK data analysis toolset. Our findings showed that 24% of the sampled Pakistani cow population are homozygous wild-type (GG), 12% homozygous mutant (TT), while 64% found heterozygous (GT). Sampled cows were obeying Hardy Weinberg Equilibrium (HWE) with{chi} 2 (2, N = 50) = 10.39, p = 0.049. Similarly, Chi-square variant association was also observed significant with p-value of 1.267x10-3 having minor-allele frequency of 0.60 and 0.28 in heighted (cases) and control cohorts respectively. Additionally, a positive odds-ratio of 3.85 is also evident that the subject variant is under-selection and showing the tendency of the mutant allele almost 4-times higher in cases vs control groups. This pilot scale study would be helpful to gain insight of variability of the subject SNP in the sampled cow population but further functional studies on larger sample size may be conducted for validation and subsequent results can be disseminated to improve this valued trait of the indigenous cows for gaining maximum milk and meat production from this esteemed species.

genetics↗

bioRxiv2023

Membrane-bound Interleukin-1α mediates leukocyte adhesion during atherogenesis

BackgroundThe interleukin-1 (IL-1) family and the NLR family pyrin domain-containing 3 (NLRP3) inflammasome contribute to atherogenesis but the underlying mechanism are incompletely understood. Unlike IL-1{beta}, IL-1 is not dependent on the NLRP3 inflammasome to exert its pro-inflammatory effects. Here, a non-genetic model was applied to characterize the role of IL-1, IL-1{beta} and NLRP3 for the pathogenesis of atherosclerosis. MethodsAtherogenesis was induced by gain-of-function PCSK9-AAV8 mutant viruses and feeding of a high-fat western diet (WTD) for 12 weeks in C57Bl6/J wildtype mice (control) and in Il1a-/-, Nlrp3-/-, and Il1b-/- mice. ResultsIl1a-/- mice showed reduced atherosclerotic plaque area in the aortic root with lower lipid accumulation, while no difference was observed between wildtype, Nlrp3-/- and Il1b-/- mice. Serum proteomic analysis showed a reduction of pro-inflammatory cytokines (e.g. IL-1{beta}, IL-6) in Il1a-/- as well as in Nlrp3-/- and Il1b-/- mice. Bone marrow dendritic cells (BMDC) of WT, Nlrp3-/- and Il1b-/- mice and primary human monocytes showed translocation of IL-1 to the plasma membrane (csIL-1) upon stimulation with LPS. The translocation of IL-1 to the cell surface was regulated by myristoylation and increased in mice with hypercholesterolemia. CsIL-1 and IL1R1 protein-protein interaction on endothelial cells induced VCAM1 expression and monocyte adhesion, which was abrogated by the administration of neutralizing antibodies against IL-1 and IL1R1. ConclusionsIl1a-/- mice, but not Nlrp3-/- or Il1b-/- mice, are protected from atherosclerosis after induction of hypercholesterolemia independent of circulating cytokines. Myristoylation and translocation of IL-1 to the cell surface in myeloid cells facilitates leukocyte adhesion and contributes to the development of atherosclerosis. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=114 SRC="FIGDIR/small/543077v1_ufig1.gif" ALT="Figure 1"> View larger version (47K): org.highwire.dtl.DTLVardef@c54814org.highwire.dtl.DTLVardef@1ff1971org.highwire.dtl.DTLVardef@df5605org.highwire.dtl.DTLVardef@889a1a_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstract.C_FLOATNO The role of cell-surface (cs) IL-1a in the initiation of atherosclerosis. C_FIG

immunology↗

bioRxiv2022

Implications of the 375W mutation for HIV-1 tropism and vaccine development.

HIV-1 vaccines need to induce broadly neutralizing antibodies (bnAb) against conserved epitopes in the envelope glycoprotein (Env) to protect against diverse HIV-1 clades. To achieve this, we need to understand how different amino acids affect the Env trimer structure to find a common strategy to readily produce Env vaccines of different subtypes. Previously, using a saturation mutagenesis strategy we identified single Env substitutions that open the CD4bs without modifying the trimer apex. One of these substitutions was a tryptophan residue introduced at position 375. Here, we introduced 375W into a large panel of 27 T/F, acute stage, chronic infection, and AIDS M-tropic, and non-M-tropic primary isolates from clades A, B, C, D and G, and circulating recombinant forms (CRFs) (CRF02_AG, and CRF01_AE), and a complex (cpx) (CRF13_cpx). To understand the effect of 375W mutation on Env trimer structure and tropism, we evaluated soluble (sCD4) and monoclonal antibody (mAb) neutralization of wt and mutant Env+ pseudovirions using bnAbs (b6, 17b, b12, VCR01, 3BNC117, PGT128, 10-1074, PGT145, PG9 and PG16), as well as macrophage infection. Broadly neutralizing Abs (bnAbs) such VCR01, and 3BNC117 neutralized almost all the primary isolates tested while the other bnAbs neutralized many but not all of our panel. In general, 375W did not impair or abrogate neutralization of potent bnAbs. However, b12 and VCR01 showed some tendencies to neutralize 375W macrophage-tropic (mac-tropic) and intermediate mac-tropic mutants more efficiently compared with non-mac-tropic mutants. We identify wt and 375W mutant Envs in our panel that infected macrophages more efficiently than non-mac-tropic variants but did not reach the levels of highly macrophage-tropic brain reference Envs. These partial mac-tropic Envs were classified as intermediate mac-tropic variants. Surprisingly, we observed a mac-tropic (clade G) and intermediate mac-tropic (clade C, and D) primary isolates wt Envs that were not derived from the central nervous system (CNS). The 375W substitution increased sensitivity to sCD4 in all Envs of our panel and increased macrophage infection in many Envs tested including a CRF01_AE X4 variant. However, variants already highly mac-tropic were compromised indicating the presence of other factors implicated in mac-tropism. Increased sCD4 sensitivity and enhanced macrophage infection provide strong evidence that 375W confers exposure of the CD4bs across Envs from different clades/CRF/cpx and disease stages. Enhanced exposure of the CD4bs by 375W had little or no effect on exposure and sensitivity of CD4bs epitopes targeted by potent bnAbs. In summary, we show that 375W consistently increases Env binding to CD4 for diverse Envs from different clades and disease stages, 375W exposure of CD4 receptor is a biologically functional substitution that alone confers mac-tropism on non-mac-tropic Envs and 3) 375W is an ideal substitution for inclusion into HIV vaccines constructed from different subtype Envs, with the aim to elicit neutralizing antibodies that target the CD4bs while maintaining exposure of other Env broad neutralization sites, and 4) we found mac-tropic and intermediate mac-tropic Envs from blood indicating that these Envs could evolve outside of CNS or be released from Brain. SignificanceSubstitutions exposing the CD4 binding site (CD4bs) on HIV-1 trimers, but still occluding non-neutralizing, immunogenic epitopes are desirable to develop HIV-1 vaccines. If such substitutions induce similar structural changes in trimers across diverse clades, they could be exploited in development of multi-clade Envelope vaccines. We show the 375W substitution increases CD4 affinity for Envelopes of all clades, circulating recombinant forms and complex Envs tested, independent of disease stage. Clade B and C Envs with an exposed CD4bs were described for macrophage-tropic strains from central nervous system (CNS). Here, we show that intermediate (clade C, and D) and macrophage-tropic (clade G) Envelopes can be detected outside CNS. Vaccines targeting the CD4bs will be particularly effective against such strains and CNS disease.

microbiology↗

bioRxiv2022

Blood-based transcriptomic signature panel identification for cancer diagnosis: Benchmarking of feature extraction methods

Liquid biopsy has shown promise for cancer diagnosis due to its minimally invasive nature and the potential for novel biomarker discovery. However, the low concentration of relevant blood-based biosources and the heterogeneity of samples (i.e. the variability of relative abundance of molecules identified), pose major challenges to biomarker discovery. Moreover, the number of molecular measurements or features (e.g., transcript read counts) per sample could be in the order of several thousand, whereas the number of samples is often substantially lower, leading to the curse of dimensionality. These challenges, among others, elucidate the importance of a robust biomarker panel identification or feature extraction step wherein relevant molecular measurements are identified prior to classification for cancer detection. In this work, we performed a benchmarking study on eleven feature extraction methods using transcriptomic profiles derived from different blood-based biosources. The methods were assessed both in terms of their predictive performance and the robustness of the biomarker panels in diagnosing cancer or stratifying cancer subtypes. While performing the comparison, the feature extraction methods are categorised into feature subset selection methods and transformation methods. A transformation feature extraction method, namely PLS-DA, was found to perform consistently superior in terms of classification performance, while a feature subset selection method, namely Ranger, selected feature sets that were the most robust to sub-sampling in terms of consistently selecting the same features. As part of the benchmarking study, a generic pipeline has been created and made available as an R package to ensure reproducibility of the results and allow for easy extension of this study to other datasets.

bioinformatics↗

bioRxiv2022

Atypical MAPK regulates translocation of GATA transcription factor in response to chemoattractant stimulation

The Dictyostelium atypical MAPK Erk2 (a.k.a. ErkB) is required for chemotactic responses to external cAMP as individual amoeba aggregate and undergo a multicellular developmental program. External cAMP also stimulates the translocation of the GATA transcription factor, GtaC, a key regulator of developmental gene expression and a developmental timer of repeated cAMP stimulation of developing cells. In this study, atypical MAPK Erk2 was found to be essential for the translocation of GtaC in response to external cAMP as indicated by the cellular distribution of GFP-GtaC reporters. Erk2 was also demonstrated to mediate the translocation of GtaC in response to external folate, a signal that directs the foraging of amoeba for bacterial food sources. Erk1, the only other Dictyostelium MAPK, was not required for the GtaC translocation to either chemoattractant, indicating that GFP-GtaC is a kinase translocation reporter specific for atypical MAPKs. The translocation of GFP-GtaC in response to folate was absent in mutants lacking the folate receptor, Far1 (a.k.a. GrlL) or the coupled G protein, G4 subunit. Loss of GtaC function resulted in enhanced chemotactic movement to folate. Inspection of the GtaC primary sequence revealed four sites recognized as Erk2 preferred phosphorylation sites. The creation and analysis of GFP-GtaC mutants with alterations at these sites determined that these sites are required for translocation in response to folate. Consistent with the role of translocation for GtaC function certain combinations of these phosphorylation site alterations interfered with the ability of GFP-GtaC reporter to rescue aggregation of gtaC- cells. These findings provide the first evidence that atypical MAPKs can regulate transcription factors through specific phosphorylation sites in response to chemoattractants. The ability of different stimuli to regulate GtaC translocation through Erk2 indicates atypical MAPKs can regulate different cell fates in part through the translocation of transcription factors.

developmental biology↗

bioRxiv2021

A novel non-genetic murine model of hyperglycemia and hyperlipidemia-associated accelerated atherosclerosis

ObjectiveAtherosclerosis, the main pathology underlying cardiovascular diseases is accelerated in diabetic patients. Genetic mouse models require breeding efforts which are time-consuming and costly. Our aim was to establish a new nongenetic model of inducible metabolic risk factors that mimics hyperlipidemia, hyperglycemia, or both and allows the detection of phenotypic differences dependent on the metabolic stressor(s). Methods and ResultsWild-type mice were injected with gain-of-function PCSK9D377Y (proprotein convertase subtilisin/kexin type 9) mutant adeno-associated viral particles (AAV) and streptozotocin and fed either a high-fat diet (HFD) for 12 or 20 weeks or a high-cholesterol/high-fat diet (Paigen diet, PD) for 8 weeks. To evaluate atherosclerosis, two different vascular sites (aortic sinus and the truncus of the brachiocephalic artery) were examined in the mice. Combined hyperlipidemic and hyperglycemic (HGHCi) mice fed a HFD or PD displayed characteristic features of aggravated atherosclerosis when compared to hyperlipidemia (HCi HFD or PD) mice alone. Atherosclerotic plaques of HGHCi HFD animals were larger, showed a less stable phenotype (measured by the increased necrotic core area, reduced fibrous cap thickness, and less -SMA-positive area) and had more inflammation (increased plasma IL-1{beta} level, aortic pro-inflammatory gene expression, and MOMA-2-positive cells in the BCA) after 20 weeks of HFD. Differences between the HGHCi and HCi HFD models were confirmed using RNA-seq analysis of aortic tissue, revealing that significantly more genes were dysregulated in mice with combined hyperlipidemia and hyperglycemia than in the hyperlipidemia-only group. The HGHCi-associated genes were related to pathways regulating inflammation (increased Cd68, iNos, and Tnfa expression) and extracellular matrix degradation (Adamts4 and Mmp14). When comparing HFD with PD, the PD aggravated atherosclerosis to a greater extent in mice and showed plaque formation after 8 weeks. Hyperlipidemic and hyperglycemic mice fed a PD (HGHCi PD) showed less collagen (Sirius red) and increased inflammation (CD68-positive cells) within aortic plaques than hyperlipidemic mice (HCi PD). HGHCi-PD mice represent a directly inducible hyperglycemic atherosclerosis model compared with HFD-fed mice, in which atherosclerosis is severe by 8 weeks. ConclusionWe established a nongenetically inducible mouse model allowing comparative analyses of atherosclerosis in HCi and HGHCi conditions and its modification by diet, allowing analyses of multiple metabolic hits in mice.

pharmacology and toxicology↗

bioRxiv2021

Sandalwood, an Indian medicinal plant attenuates the microbial growth and influence up/down regulation of the metabolites

The methanolic extract of sandalwood (SwME) was prepared by soxhlet apparatus and the antibacterial assay was performed. Further, the metabolite profiling of SwME and lysates of E. coli and E. coli grown in the presence of SwME was generated. SwME showed maximum inhibition against E. coli (MTCC 443) i.e. 82.71%, and minimal against B. subtilis (MTCC 736) i.e. 26.82%. The metabolome profiles of E. coli and SwME were generated using gas chromatography-mass spectrometry (GC-MS) technique. Comparative studies were done to understand to what extent metabolite modifications differ between SwME, E. coli lysate and the E. coli strain grown in presence of extract. Result revealed 23 peaks with major compounds present in E. coli were 9-Octadecenoic Acid (Z)-, Methyl Ester (26.85%), Hexadecanoic Acid, methyl ester (20.5%) and Hexadecanoic acid, trimethylsilyl ester (15.79%). When E. coli was grown in the presence of SwME, GC-MS analysis showed 25 peaks with major compounds such as 9-Octadecenoic Acid, Methyl Ester (21.97%), Hexadecanoic Acid, Methyl Ester (17.03%), and Hexadecanoic Acid, Trimethylsilyl Ester (14.96%). Correlating the metabolic profiles with the changes occurring is essential to progression their comprehension and in the development of new approaches to identify the metabolomics regulation in E. coli in response to SwME.

microbiology↗