Biology subjects

Klahn, P.

Publications and source records attributed to Klahn, P..

3 recordsLinked to original sources

bioRxiv2026

Rapid Host Plant Adaptation via Ectopic Gene Conversion in Plutellid Moths

Herbivorous insects face an extraordinary challenge: the chemical defenses of their host plants are highly diverse, rapidly evolving, and largely unpredictable. How insects meet this challenge remains poorly understood. Here we show that ectopic gene conversion (EGC) has repeatedly driven the evolutionary diversification of glucosinolate sulfatases (GSSs), the key larval counteradaptation in plutellid moths to glucosinolate based defenses in cruciferous plants. Across seven plutellid species, enzyme assays with heterologously expressed GSSs and 21 glucosinolates revealed distinct activity profiles: GSSs from species with broad host ranges within glucosinolate-containing plants showed balanced activity across substrates, whereas GSSs from specialists displayed profiles biased toward the glucosinolate composition of their host plants. Comparative genomic analyses identified extensive conversion among duplicated genes, both historically across the clade and in contemporary Plutella armoraciae. In this originally monophagous species, EGC-mediated diversification of GSS enzymes coincides with the rapid inclusion of a new cruciferous host within <200 years, demonstrating the potential of EGC to drive host-range expansion on strikingly short evolutionary timescales. Structural modelling and molecular dynamics simulations further support functional shifts in GSS enzymes arising from EGC-derived sequence alterations. Together, these results demonstrate that EGC provides a powerful mechanism for fine tuning detoxification enzymes, enabling herbivorous insects to adapt to chemically diverse host plants despite constrained enzymatic toolkits.

evolutionary biology↗

bioRxiv2025

Controlled Delivery and Light-Induced Release of Magic Spot Nucleotides in Escherichia coli

The "magic spot nucleotides" (MSNs) ppGpp and pppGpp (also: (p)ppGpp) are bacterial alarmones central to the conserved stringent response, a stress adaptation mechanism that helps bacteria adapt to stress conditions and hostile environments. Current strategies to manipulate MSN levels rely mainly on genetic or environmental approaches, which are slow and lack temporal control. Chemical tools such as photocaged MSN analogues could provide such temporal control over MSN levels. However, the high negative charge of MSNs prevents spontaneous passage through the complex bacterial cell envelope. Here, we report the synthesis of photocaged, clickable, and isotope-labeled MSN analogues and their delivery into Escherichia coli comparing different approaches. A cyclodextrin-based synthetic nucleotide transporter provides particular advantages. Upon 400 nm irradiation, these probes were photo-released inside living cells, where we tracked their conversion from pppGpp to ppGpp by capillary electrophoresis mass spectrometry and studied their ability to alter growth in a (p)ppGpp0 mutant. This work provides the first demonstration that highly charged, photocaged MSNs can traverse the bacterial envelope, be photo-released intracellularly, and be metabolically tracked in real time. These probes lay the foundation for spatially and temporally controlled studies of MSN function and of other highly negatively charged metabolites in bacteria.

biochemistry↗

bioRxiv2025

MAIT cells protect in severe pneumococcal pneumonia by regulating neutrophil/macrophage antimicrobial activities

Mucosal-Associated Invariant T (MAIT) cells populate the lung tissue where they contribute to defense against respiratory infections. While MAIT cells have been implicated in host resistance to infections caused by Gram-negative bacteria, their contribution in immunity against Gram-positive bacteria-driven pneumonia is still enigmatic. Here, we demonstrate that both mouse and human MAIT cells are activated during severe infection caused by Streptococcus pneumoniae, the major cause of community-acquired bacterial pneumonia. Upon infection, lung MAIT cells undergo a transcriptional reprogramming associated with acquisition of potent antimicrobial properties. MAIT cell-deficient mice are more susceptible to pneumococcal pneumonia, including higher mortality, uncontrolled bacterial growth and dissemination, and impaired neutrophil and interstitial macrophage activity. Moreover, prophylactic stimulation of MAIT cells using cognate antigen protects from pneumococcus-induced lethal pneumonia. These findings demonstrate that MAIT cells are key cellular actors during Gram-positive bacterial infections.

immunology↗