Biology subjects

Brandstetter, M.

Publications and source records attributed to Brandstetter, M..

3 recordsLinked to original sources

bioRxiv2024

Detection of Unlabeled Micro- and Nanoplastics in Unstained Tissue with Optical Photothermal Infrared Spectroscopy

In this study, we investigate the efficacy of Optical Photothermal Infrared (O-PTIR) spectroscopy, also known as mid-infrared photothermal (MIP) microscopy, for the detection of micro- and nano plastics (MNPs) down to diameters of 250 nm in mammalian tissues. Experiments with both in vitro 3D cell cultures derived from HTC116 colorectal cancer cell line and in vivo mouse tissue models were conducted to evaluate the spatial resolution limits and quality of spectra that formed the basis for label-free and non- destructive identification of MNPs. Our findings demonstrate the superior resolution of O-PTIR in imaging individual particles of 250 nm in mouse kidney tissues, surpassing the capabilities of traditional FTIR spectroscopy, which was applied as a reference technique. Furthermore, we introduce a semi-automated image analysis that incorporates machine learning algorithms to accelerate the detection process, thus improving throughput and minimizing the potential for human error. The results confirm that O-PTIR produces high-quality, artefact-free spectral images in a contact-less manner and significantly outperforms FTIR in terms of spatial resolution and signal-to-noise ratio in complex biological matrices.

biophysics↗

bioRxiv2024

Increase in ER-mitochondria contacts and mitochondrial fusion are hallmarks of mitochondrial activation during embryogenesis

Mitochondrial ATP production is essential for development, yet the mechanisms underlying the continuous increase in mitochondrial activity during embryogenesis remain elusive. Using zebrafish as a model system for vertebrate development, we comprehensively profile mitochondrial activity, morphology, metabolome, proteome and phospho-proteome as well as respiratory chain enzymatic activity. Our data show that the increase in mitochondrial activity during embryogenesis does not require mitochondrial biogenesis, is not limited by metabolic substrates at early stages, and occurs without an increase in the abundance of respiratory chain complexes or their in vitro activity. Our analyses pinpoint a previously unexplored increase in mitochondrial-ER association during early stages in combination with changes in mitochondrial morphology at later stages as possible contributors to the rise in mitochondrial activity during embryogenesis. Overall, our systematic profiling of the molecular and morphological changes to mitochondria during embryogenesis provides a valuable resource for further studying mitochondrial function during embryogenesis.

developmental biology↗

bioRxiv2020

A deeply conserved miR-1 dependent regulon supports muscle cell physiology

Muscles are not only essential for force generation but are also key regulators of systemic energy homeostasis1. Both these roles rely heavily on mitochondria and lysosome function as providers of energy and building blocks, but also as metabolic sensors2-4. Perturbations in these organelles or their crosstalk lead to a wide range of pathologies5. Here, we uncover a deeply conserved regulon of mitochondria and lysosome homeostasis under control of the muscle-specific microRNA miR-1. Animals lacking miR-1 display a diverse range of muscle cell defects that have been attributed to numerous different targets6. Guided by the striking conservation of miR-1 and some of its predicted targets, we identified a set of direct targets that can explain the pleiotropic function of miR-1. miR-1-mediated repression of multiple subunits of the vacuolar ATPase (V-ATPase) complex, a key player in the acidification of internal compartments and a hub for metabolic signaling7,8, and of DCT-1/BNIP3, a mitochondrial protein involved in mitophagy and apoptosis9,10, accounts for the function of this miRNA in C. elegans. Surprisingly, although multiple V-ATPase subunits are upregulated in the absence of miR-1, this causes a loss-of-function of V-ATPase due to altered levels or stoichiometry, which negatively impact complex assembly. Finally, we demonstrate the conservation of the functional relationship between miR-1 and the V-ATPase complex in Drosophila.

cell biology↗