Biology subjects

Witwicka, A.

Publications and source records attributed to Witwicka, A..

4 recordsLinked to original sources

bioRxiv2025

Minimal overlaps in responses to insecticides between pollinator species

Insecticides are important for protecting crops from agricultural pests, yet their use inadvertently drives global declines in beneficial insects, including pollinators. Insecticide regulation relies on the assumption that model bee species adequately represent responses to exposure across the diversity of insect taxa, despite over 479 million years of evolutionary divergence and a limited understanding of how exposure effects vary across insect orders. Here, using comparative whole-brain transcriptomics, we show differences in molecular responses to modern insecticides across evolutionary distant pollinator lineages: butterflies, flies, and bees. Within each of the four species studied, different insecticides (sulfoxaflor and clothianidin) triggered broadly similar gene regulatory responses. In surprising contrast, exposure impacts differed sharply among species, with no genes or pathways being consistently affected. Strikingly, we found that sulfoxaflor, approved based on its supposed safety for bees, causes more disruptions in non-bee pollinators than the restricted neonicotinoid clothianidin, revealing a critical blind spot in current assessment protocols. Our findings demonstrate that over large evolutionary timescales, species-level differences can outweigh variations in insecticide chemical structures in shaping the effects of insecticide exposure. These interspecific differences likely reflect distinct physiological and metabolic traits shaped over tens to hundreds of millions of years. Together, our findings highlight the urgent need to reevaluate insecticide safety assessments to incorporate phylogenetic diversity, potentially explaining why regulatory efforts have failed to halt pollinator declines despite stricter testing requirements. Significance StatementInsecticide regulations are based on a narrow set of test species, overlooking the evolutionary and functional diversity among pollinators. Here, we show that molecular responses to insecticides differ more between species than between chemicals, even when targeting the same neural receptors. Strikingly, an insecticide considered safe for bees caused greater molecular disruption in non-bee pollinators. Our findings challenge current assumptions in pesticide risk assessment and suggest that using surrogate species can misrepresent broader ecological risks. By revealing species-specific vulnerabilities rooted in millions of years of divergent evolution, this study underscores the need for a more inclusive and phylogenetically informed approach to protecting pollinator biodiversity.

evolutionary biology↗

bioRxiv2024

Acute and chronic pesticide exposure trigger fundamentally different molecular responses in bumble bee brains

Beneficial wild insects including pollinators encounter various pesticide exposure conditions, from brief high concentrations to continuous low-level exposure. To effectively assess the environmental risks of pesticides, it is critical to understand how different exposure patterns influence their effects. Unfortunately, this knowledge remains limited. To clarify whether different exposure schemes disrupt the physiology of pollinators in similar manners, we exposed bumble bees to acute and chronic treatments of three different pesticides: Acetamiprid, clothianidin, and sulfoxaflor. Gene expression profiling enabled us to compare the effects of these treatments on the brain in a high-resolution manner. There were two main surprises: First, acute and chronic exposure schemes affected largely non-overlapping sets of genes. Second, different pesticides under the same exposure scheme showed more comparable effects than the same pesticide under different exposure schemes. Acute exposure caused up-regulation of stress response mechanisms causing distinct regulatory changes, rather than amplifying the effects of prolonged low-dose exposure that affected predominantly immunity and energy metabolism. These findings show that the mode of exposure critically determines the effects of pesticides. Our results signal the need for safety testing practices to better consider mode-of-exposure dependent effects and suggest that transcriptomics can support such improvements.

ecology↗

bioRxiv2024

A neonicotinoid pesticide causes tissue-specific gene expression changes in bumble bees

Pesticides often harm beneficial insect pollinators, impairing their ability to navigate the environment, learn, fight off disease, and reproduce. Understanding the mechanisms behind these disorders is essential for improving pesticide risk assessments. To test whether pesticide exposure induces similar or distinct transcriptional responses across tissues, we administered field-realistic dose of the common neonicotinoid clothianidin to Bombus terrestris bumble bees. We then measured gene expression in brains, hind femurs, and Malpighian tubules. Our analyses revealed that 82% of gene expression differences were tissue-specific. Although genes associated with energy metabolism were consistently down-regulated across all tissues, pesticide exposure primarily affected core tissue functions, namely genes linked to ion transport in the brain, muscle function in the hind femur, and detoxification in Malpighian tubules. Furthermore, while the brain holds the highest abundance of pesticide target receptors, other tissues showed more substantial differences in gene expression magnitude. These findings reveal that pesticide exposure causes complex, tissue-specific effects rather than a uniform body-wide response. Our study provides a mechanistic basis for the severe effects of pesticide exposure on bees and shows how transcriptomics can help pinpoint the most affected areas and processes across the body. Accordingly focusing toxicological assays could significantly improve the precision of pesticide safety evaluations.

ecology↗

bioRxiv2021

Parameter exploration improves the accuracy of long-read genome assembly

Long-molecule sequencing is now routinely applied to generate high-quality reference genome assemblies. However, datasets differ in repeat composition, heterozygosity, read lengths and error profiles. The assembly parameters that provide the best results could thus differ across datasets. By integrating four complementary and biologically meaningful metrics, we show that simple fine-tuning of assembly parameters can substantially improve the quality of long-read genome assemblies. In particular, modifying estimates of sequencing error rates improves some metrics more than two-fold. We provide a flexible software, CompareGenomeQualities, that automates comparisons of assembly qualities for researchers wanting a straightforward mechanism for choosing among multiple assemblies.

bioinformatics↗