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Borowiec, M.

Publications and source records attributed to Borowiec, M..

2 recordsLinked to original sources

Understanding cryptic diversity within the honeypot ant species complex of Myrmecocystus mendax

Cryptic species diversity, overlooked due to extreme morphological similarity, is a common phenomenon among ants. The "honeypot ant" genus Myrmecocystus (Wesmael, 1838; Formicinae: Lasiini) likely features multiple cryptic species, as previously suggested by phylogenetic studies based on ultraconserved elements (UCEs). Here, this work is expanded upon by examining 140 specimens and 2,508 UCE loci, with a particular focus on the M. mendax species complex from the southwestern USA and northern Mexico. Phylogenomic and population genomic analyses revealed five distinct M. mendax-like lineages and identified two potential cases of cryptic species diversity, one within samples matching the morphology of M. mendax and another within samples conforming to M. placodops. Most specimens morphologically identified as M. mendax formed a well-supported monophyletic group sister to M. melliger assigned individuals, with evidence for ongoing hybridization between both species in the Madrean Sky Islands along the USA-Mexico border. Patterns in the main M. mendax clade also suggest adaptive divergence across ecological gradients, warranting further investigation. Overall, these findings highlight the power of UCE-based genomic data in phylogenetic reconstructions and population genetic analyses to better resolve cryptic species diversity, and clarify complex evolutionary histories shaped by introgression and incomplete lineage sorting.

genomics↗

BRG1 targeting overcomes ABCC-based multidrug resistance induced by paclitaxel

Multidrug resistance of cancer cells is attributed to drug-induced alteration of numerous intracellular processes. Using clinically relevant models of triple-negative breast and non-small lung cancer cells we previously showed that these cells respond to repeated paclitaxel exposure by inter alia lysosome enrichment in ABCC3, ABCC5 and ABCC10, which contribute to drug sequestration in these organelles and reduced drug cytotoxicity. In this study we provide experimental evidence that transcription of above mentioned ABCC genes is enabled by BRG1-based SWI/SNF chromatin remodeling complex. Pharmacological inhibition of SWI/SNF with PFI3 or ACBI1, the PROTAC degrader of SMARCA2/4, substantially decline transcription of ABCC3, ABCC5 and ABCC10. Similar effect is caused by transient silencing of SMARCA4 (BRG1), but not SMARCA2 (BRM). The deficiency of BRG1 led to extralysosomal distribution of anticancer drugs, their deeper penetration of spheroids and substantial increase in drug cytotoxicity. Interestingly, in BRG1 deficient cell line paclitaxel triggered mutations, which reverted BRG1 truncating deletion in SMARCA4, thereby restoring SWI/SNF ATPase expression in paclitaxel-resistant cells and increasing transcription of ABCC. Acquisition of drug resistance was associated with BRG1 redistribution in the genome, de novo occurrence at the promoters of genes functionally linked to endo-lysosomal system and stronger co-occurrence with EP300. Our study indicates possible target - SWI/SNF complex for anticancer combinatorial interventions in paclitaxel-induced multidrug resistant phenotypes.

cancer biology↗