Biology subjects

Bagchi, R.

Publications and source records attributed to Bagchi, R..

4 recordsLinked to original sources

bioRxiv2025

Influence of natural enemy specificity and functional response on victim coexistence

Natural enemies are thought to promote coexistence of competing victim species. Although existing theory suggests victim coexistence increases with enemy specialization, the dynamics and potential extinction of enemies is generally discounted. Where enemy dynamics have been considered, empirically atypical linear functional responses have been studied. These limitations could over-simplify inferences about enemy-mediated coexistence. We studied the dynamics of two competing victim species and two enemy species with a deterministic model. We derived equilibrium points, and used linear stability analysis, numerical simulations and Floquet theory to determine the influence of enemy specificity and non-linear functional responses on coexistence in this victim-enemy community. We found greater specificity could drive enemy equilibrium points to infeasible values. We found only accelerating enemy functional responses result in stable equilibrium point coexistence of otherwise equivalent competitor victims, in which case greater specificity results in greater stability. Linear and saturating responses produce complex dynamics (neutral or limit cycles, chaos) or extinction, with limit cycle stability highest at intermediate specificity. Our results indicate strict specificity may not maximize coexistence, and enemy functional response critically influences whether enemies promote victim coexistence. They highlight the need to incorporate enemy dynamics into the growing body of theory regarding enemy-mediated diversity maintenance.

ecology↗

bioRxiv2022

Understandable Multifunctionality Measures Using Hill Numbers

In ecology, multifunctionality measures the simultaneous performance of multiple ecosystem functions. If species diversity describes the variety of species that together build the ecosystem, multifunctionality attempts to describe the variety of functions these species perform. A range of methods have been proposed to quantify multifunctionality, successively attempting to alleviate problems that have been identified with the previous methods. This has led to a proliferation of more-or-less closely related metrics which, however, lack an overarching theoretical framework. Here we borrow from the comprehensive framework of species diversity to derive a new metric of multifunctionality. Analogously to the effective number of species used to quantify species diversity, the metric we propose is influenced both by the number of functions as well as, crucially, the evenness of performance levels across functions. In addition, the effective multifunctionality also considers the average level at which the functions are performed. The result is a measure of the cumulative performance of the system were all functions provided equally. The framework allows for the inclusion of the correlation structure among functions, thus allowing it to account for non-independence between functions. We show that the average metric is a special case of the newly proposed metric when all functions are uncorrelated and performed at equal levels. We hope that by providing a new metric of multifunctionality anchored in the rigorous framework of species diversity based on effective numbers, we will overcome the considerable skepticism that the larger community of ecologists has built against indices of multifunctionality. We thereby hope to help popularize this important concept which, as biological diversity, describes a fundamental property of ecosystems and thus lies at the heart of ecology.

ecology↗

bioRxiv2021

Polyvalent Guide RNAs for CRISPR Antivirals

CRISPR biotechnologies, where CRISPR effectors recognize and degrade specific nucleic acid targets that are complementary to their guide RNA (gRNA) cofactors, have been primarily used as a tool for precision gene editing1 but possess an emerging potential for novel antiviral diagnostics, prophylactics, and therapeutics.2-5 In gene editing applications, significant efforts are made to limit the natural tolerance of CRISPR effectors for nucleic acids with imperfect complementarity to their gRNAs in order to prevent degradation and mutation at unintended or "off-target" sites; here we exploit those tolerances to engineer gRNAs that are optimized to promote activity at multiple viral target sites, simultaneously, given that multiplexed targeting is a critical tactic for improving viral detection sensitivity,3 expanding recognition of clinical strain variants,6 and suppressing viral mutagenic escape from CRISPR antivirals.7 We demonstrate in vitro and in higher plants that single "polyvalent" gRNAs (pgRNAs) in complex with CRISPR effectors Cas9 or Cas13 can effectively degrade pairs of viral targets with significant sequence divergence (up to 40% nucleotide differences) that are prevalent in viral genomes. We find that CRISPR antivirals using pgRNAs can robustly suppress the propagation of plant RNA viruses, in vivo, better than those with a "monovalent" gRNA counterpart. These results represent a powerful new approach to gRNA design for antiviral applications that can be readily incorporated into current viral detection and therapeutic strategies, and highlight the need for specific approaches and tools that can address the differential requirements of precision gene editing vs. CRISPR antiviral applications in order to mature these promising biotechnologies.

bioengineering↗

bioRxiv2020

Suppression of canonical TGF-β signaling enables GATA4 to interact with H3K27me3 demethylase JMJD3 to promote cardiomyogenesis

Direct reprogramming of fibroblasts into cardiomyocytes (CMs) represents a promising strategy to regenerate CMs lost after ischemic heart injury. Overexpression of GATA4, HAND2, MEF2C, TBX5, miR-1, and miR-133 (GHMT2m) along with transforming growth factor beta (TGF-{beta}) inhibition efficiently promotes reprogramming. However, the mechanisms by which TGF-{beta} blockade promotes cardiac reprogramming remain unknown. Here, we identify interactions between the histone H3 lysine 27 trimethylation (H3K27me3) - demethylase JMJD3, the SWI/SNF remodeling complex subunit BRG1, and cardiac transcription factors. Furthermore, canonical TGF-{beta} signaling regulates the interaction between GATA4 and JMJD3. TGF-{beta} activation impairs the ability of GATA4 to bind target genes and prevents demethylation of H3K27 at cardiac gene promoters during cardiac reprogramming. Finally, a mutation in GATA4 (V267M) exhibits reduced binding to JMJD3 and impaired cardiomyogenesis. Thus, we have identified an epigenetic mechanism wherein canonical TGF-{beta} pathway activation impairs cardiac gene programming by interfering with GATA4-JMJD3 interactions.

cell biology↗