Biology subjects

Braendle, F.

Publications and source records attributed to Braendle, F..

3 recordsLinked to original sources

bioRxiv2026

Nuclear stress bodies enable a germline-specific transcriptional stress response in Drosophila

The germline ensures the continuity of genetic information across generations, but how this immortal lineage functions under stress conditions remains incompletely understood. Here, we identify that heat shock factor (Hsf), a conserved master regulator of the stress response, drives the expression of transposable elements (TEs), in addition to molecular chaperones upon heat shock in Drosophila gonads. In germ cells, this potential intra-genomic conflict is countered by the formation of nuclear stress bodies (nSBs) at non-coding satellite DNA repeats. Using chemical and genetic perturbations, we demonstrate that nSBs are both necessary and sufficient to delay Hsf-dependent transcription. Notably, this nSB-mediated delay, in tandem with the piRNA pathway, allows germ cells to selectively express molecular chaperones, but not transposable elements, upon heat shock. Overall, we propose that this unique transcriptional stress response preserves germline function and evolutionary fitness, especially in natural populations routinely exposed to environmental stress.

cell biology↗

bioRxiv2026

Novel Protoporphyrinogen oxidase 1 mutations endow resistance to PPO-inhibiting herbicides in Bassia scoparia

PPO-inhibiting herbicides are widely used to manage weeds in different cropping systems, yet resistance evolution threatens their long-term efficacy. Here, we investigated the molecular basis of resistance to PPO-inhibiting herbicides in Bassia scoparia biotypes collected from four locations in North Dakota, USA. Greenhouse dose-response assays revealed high levels of resistance to saflufenacil and carfentrazone-ethyl, while fomesafen retained full efficacy across all biotypes. Resistant plants did not show increased copy number or elevated expression of PPO1 or PPO2. Sequencing of survivor plants revealed conserved PPO2 sequences, but consistent target-site substitutions at position F454 in PPO1, including F454I, F454L, and F454V. In vitro enzyme assays demonstrated that these substitutions impair PPO1 sensitivity to saflufenacil and carfentrazone-ethyl, but not to fomesafen. Ectopic expression of B. scoparia PPO1 F454 mutant variants in Arabidopsis thaliana conferred tolerance to saflufenacil and carfentrazone-ethyl, but not to fomesafen, supporting greenhouse and in vitro results. Molecular modeling indicated that the conformational flexibility and interaction profile of fomesafen enables it to maintain binding to mutated PPO1 variants, in contrast to the more rigid structures of saflufenacil and carfentrazone-ethyl. A yeast-based complementation system further confirmed that F454 substitutions decrease herbicide sensitivity. In addition, developmental profiling showed distinct expression patterns of PPO1 and PPO2 during early growth stages in B. scoparia and Amaranthus spp., highlighting isoform-specific roles. Together, these findings represent the first reported PPO1 target-site mutations in a broadleaf weed species as a key mechanism of resistance and highlight that fomesafen is effective to control resistant B. scoparia populations.

biochemistry↗

bioRxiv2023

Multi-tissue proteomics identifies a link between satellite DNA organization and transgenerational transposon repression in Drosophila

Non-coding satellite DNA repeats are abundant at the pericentromeric heterochromatin of eukaryotic chromosomes. During interphase, sequence-specific DNA-binding proteins cluster these repeats from multiple chromosomes into nuclear foci known as chromocenters. Despite the pivotal role of chromocenters in cellular processes like genome encapsulation and gene repression, the associated proteins remain incompletely characterized. Here, we use two satellite DNA-binding proteins, D1 and Prod, as baits to characterize the chromocenter-associated proteome in Drosophila embryos, ovaries, and testes through quantitative mass spectrometry. We identify D1- and Prod-associated proteins, including known heterochromatin proteins as well as proteins previously unlinked to satellite DNA or chromocenters, thereby laying the foundation for a comprehensive understanding of cellular functions enabled by satellite DNA repeats and their associated proteins. Interestingly, we find that multiple components of the transposon-silencing piRNA pathway are associated with D1 and Prod in embryos. Using genetics, transcriptomics, and small RNA profiling, we show that flies lacking D1 during embryogenesis exhibit transposon expression and gonadal atrophy as adults. We further demonstrate that this gonadal atrophy can be rescued by mutating the checkpoint kinase, Chk2, which mediates germ cell arrest in response to transposon mobilization. Thus, we reveal that a satellite DNA-binding protein functions during embryogenesis to silence transposons, in a manner that is heritable across later stages of development.

cell biology↗