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Biology subjects

Shankar, N.

Publications and source records attributed to Shankar, N..

7 recordsLinked to original sources

A MultiOmics time-resolved systems map of gene regulation in Toxoplasma gondii

Understanding how T. gondii builds an invasion-competent cell has been limited by its rapid, asynchronous division cycle, incomplete gene function annotation, and studies that have examined one regulator or complex at a time. Here, we placed acute perturbation of 21 transcriptional and epigenetic factors, promoter occupancy, chromatin accessibility, and molecular validation on a common single-cell clock. The resulting consensus map links the lytic-cycle programs to candidate activating and repressive inputs, organizes genes into 108 co-regulated communities, and nominates regulatory partnerships that would not have emerged from any single data type. The work bridges three longstanding gaps: it resolves perturbation responses in cell-cycle time, distinguishes promoter occupancy from perturbation-linked regulation, and turns a large multidimensional dataset into an experimentally navigable map. We indeed confirmed known factor interactions such as MORC/HDAC3 and recovered combinations such as the Cdc5/SNIP1 and DMAP1/EPL1 as coregulatory nodes (that in other systems have been described to cooperate). Furthermore, we discovered a novel apicomplexan specific combination of AAF1/AP2XI-5 that provides mechanistic insights of the unique AP2 transcription factor family.

microbiology↗

Glutamine Metabolism Supports α cell Mass and Glucagon Secretion

The liver- cell axis is a finely tuned biological rheostat that regulates whole body amino acid availability. Pancreatic cells secrete glucagon that regulates amino acid catabolism through gluconeogenesis and ureagenesis, yet the mechanisms linking amino acid levels to cell growth and function are not fully understood. Here, we identify glutaminase, the enzyme that catalyzes glutamine catabolism, as a critical cell regulator. Glutaminase is highly enriched in cells across species. cell expression of glutaminase is required for nutrient-dependent mTORC1 activation, suppression of AMPK signaling, and sustained expression of the glutamine transporter SLC38A5. This establishes a feed-forward loop linking glutamine metabolism to amino acid sensing and growth. Reduced glutaminase activity impairs dynamic glucagon secretion in response to low glucose and amino acids. Together, these findings highlight the importance of glutamine metabolism in cell growth and hormone secretion and suggest it may play a role in cell adaptation to hyperaminoacidemia.

physiology↗

Antagonistic and Synergistic Roles of Tomato AFP3 Isoforms in Hormonal Regulation and Development

The ABA INSENSITIVE5 BINDING PROTEIN (AFP) family plays a critical role in abscisic acid (ABA) signaling through interaction with the transcription factor ABI5, impacting seed germination and stress responses. Here, we characterize tomato AFP3, which produces two isoforms: a full-length protein and a shorter microProtein (sAFP3) containing only the C-terminal domain. Functional analyses reveal contrasting roles of these isoforms in development; while AFP3 overexpression accelerates shoot growth but impairs seed germination, both afp3 loss-of-function and sAFP3-expressing mutants (afp3-D) exhibit stunted growth and developmental defects. Transcriptome profiling highlights that AFP3 and sAFP3 differentially regulate hormone-related pathways, including salicylic acid, gibberellic acid, and jasmonic acid metabolism. Proteomic interaction studies demonstrate that AFP3 and sAFP3 physically interact, sharing partners involved in hormone signaling. Hormone quantification confirms that AFP3 modulates multiple phytohormones, with elevated ABA in afp3-D mutants and increased gibberellic acid, jasmonic acid, and salicylic acid in both afp3 and afp3-D mutant backgrounds. Moreover, AFP3 controls flower and fruit development, influencing yield and ripening. Together, these findings identify AFP3 as a key integrator of hormonal crosstalk that coordinates growth, development, and stress responses in tomato. The production of dual AFP3 isoforms through alternative transcription, combined with microProtein-mediated dominant-negative regulation, reveals a sophisticated mechanism for dynamically fine-tuning transcriptional networks. This versatile strategy underscores how plants--and potentially other organisms--achieve precise control over complex signaling pathways.

plant biology↗

Impaired complement regulation drives chronic lung allograft dysfunction after lung transplantation.

A greater understanding of chronic lung allograft dysfunction (CLAD) pathobiology, the primary cause of mortality after lung transplantation, is needed to improve outcomes. The complement system links innate to adaptive immune responses and is activated early post-lung transplantation to form the C3 convertase, a critical enzyme that cleaves the central complement component C3. We hypothesized that LTx recipients with a genetic predisposition to enhanced complement activation have worse CLAD-free survival mediated through increased adaptive alloimmunity. We interrogated a known functional C3 polymorphism (C3R102G) that increases complement activation through impaired C3 convertase inactivation in two independent LTx recipient cohorts. C3R102G, identified in at least one out of three LTx recipients, was associated with worse CLAD-free survival, particularly in the subset of recipients who developed donor-specific antibodies (DSA). In a mouse orthotopic lung transplantation model, impaired recipient complement regulation resulted in more severe obstructive airway lesions when compared to wildtype controls, despite only moderate differences in graft-infiltrating effector T cells. Impaired complement regulation promoted the intragraft accumulation of memory B cells and antibody-secreting cells, resulting in increased DSA levels. In summary, genetic predisposition to complement activation is associated with B cell activation and worse CLAD-free survival. BRIEF SUMMARYLung transplant recipients genetically predisposed to impaired complement regulation demonstrate worse chronic rejection-free survival. This phenotype is associated with intragraft B cell-activation and donor-specific antibodies.

immunology↗

Multi-Generation Selection of Rhizosphere Ecosystem Associated with Plant Genotype and Biomass in Arabidopsis thaliana

The role of the microbiome in shaping the host phenotype has emerged as a critical area of investigation, with implications in ecology, evolution, and host health. The complex and dynamic interactions involving plants and their diverse rhizosphere microbial communities are influenced by a multitude of factors, including but not limited to soil type, environment, and plant genotype. Understanding the impact of these factors on microbial community assembly is key to yielding host-specific and robust benefits for plants, yet remains challenging. Here we ran an artificial ecosystem selection experiment, over eight generations, in Arabidopsis thaliana Ler and Cvi to select soil microbiomes associated with higher or lower biomass of the host. This resulted in divergent microbial communities, shaped by a complex interplay between random environmental variations, plant genotypes, and biomass selection pressures. In the initial phases of the experiment, the genotype and the biomass selection treatment have modest but significant impacts. Over time, the plant genotype and biomass treatments gain more influence, explaining [~]40% of the variation in the microbial community composition. Furthermore, a genotype-specific association of a plant growth-promoting rhizobacterial taxa, Labraceae with Ler and Rhizobiaceae with Cvi, is observed under selection for high biomass.

ecology↗

MIR319C and its target JAW-TCPs repress each other and establish cell proliferation pattern in incipient leaf primordia in Arabidopsis thaliana

The microRNA miR319 and its target JAW-TCP transcription factors regulate leaf morphogenesis in diverse plant species. In young Arabidopsis leaf primordia, JAW-TCPs are detected towards the distal region whereas MIR319C is expressed at the base. Little is known about how this complementary expression pattern of MIR319C and JAW-TCPs is generated. Here, we show that MIR319C is initially expressed uniformly throughout the incipient primordia and is later abruptly down-regulated at the distal region, with concomitant distal appearance of JAW-TCPs, when leaves grow to [~]100 {micro}m long. Loss of JAW-TCPs causes distal extension of MIR319C expression domain, whereas ectopic TCP activity restricts MIR319C more proximally. JAW-TCPs are recruited to and are capable of depositing histone H3K27me3 repressive marks on the MIR319C chromatin. JAW-TCPs fail to repress MIR319C in transgenic seedlings where the TCP-binding cis-elements on MIR319C are mutated, causing miR319 gain-of-function-like phenotype. Based on these results, we propose a model for growth patterning in leaf primordia wherein MIR319C and JAW-TCPs repress each other and divide the uniformly growing primordia into distal differentiation zone and proximal proliferation domain. Summary statementJAW-TCPs transcriptionally repress the microRNA319 encoding gene MIR319C to generate their mutually exclusive expression pattern and establish growth polarity during early stages of Arabidopsis leaf primordia.

plant biology↗

Highly functional virus-specific cellular immune response in asymptomatic SARS-CoV-2 infection

The efficacy of virus-specific T cells in clearing pathogens involves a fine balance between their antiviral and inflammatory features. SARS-CoV-2-specific T cells in individuals who clear SARS-CoV-2 infection without symptoms or disease could reveal non-pathological yet protective characteristics. We therefore compared the quantity and function of SARS-CoV-2-specific T cells in a cohort of asymptomatic individuals (n=85) with that of symptomatic COVID-19 patients (n=76), at different time points after antibody seroconversion. We quantified T cells reactive to structural proteins (M, NP and Spike) using ELISpot assays, and measured the magnitude of cytokine secretion (IL-2, IFN-{gamma}, IL-4, IL-6, IL-1{beta}, TNF- and IL-10) in whole blood following T cell activation with SARS-CoV-2 peptide pools as a functional readout. Frequencies of T cells specific for the different SARS-CoV-2 proteins in the early phases of recovery were similar between asymptomatic and symptomatic individuals. However, we detected an increased IFN-{gamma} and IL-2 production in asymptomatic compared to symptomatic individuals after activation of SARS-CoV-2-specific T cells in blood. This was associated with a proportional secretion of IL-10 and pro-inflammatory cytokines (IL-6, TNF- and IL-1{beta}) only in asymptomatic infection, while a disproportionate secretion of inflammatory cytokines was triggered by SARS-CoV-2-specific T cell activation in symptomatic individuals. Thus, asymptomatic SARS-CoV-2 infected individuals are not characterized by a weak antiviral immunity; on the contrary, they mount a robust and highly functional virus-specific cellular immune response. Their ability to induce a proportionate production of IL-10 might help to reduce inflammatory events during viral clearance.

immunology↗