Biology subjects

Giannopoulos, P.

Publications and source records attributed to Giannopoulos, P..

3 recordsLinked to original sources

bioRxiv2026

How Mitochondria Distribute and Align in HeLa Cells: A Computational Analysis On Electron Microscopy Images.

This paper investigates the way in which mitochondria distribute and align inside HeLa cells observed with serial block-face scanning electron microscopy. Four models of alignment were considered: (1) mitochondria exhibiting no discernible alignment pattern, (2) mitochondria aligned pointing towards the nucleus of the cell, (3) mitochondria aligned all in one direction when viewed from above, (4) mitochondria aligned tangent to the surface of the nucleus. These models were named (1) unaligned, (2) petals, (3) racecars, and (4) clouds. The mitochondria, nucleus and plasma membrane of 25 individual cells were segmented. A total of 12,299 mitochondria were identified and analysed. Alignment of the major axis of each mitochondrion was calculated in two ways: relative to a ray that joins it to the centroid of the nucleus, and relative to a ray that joins it to the nucleus surface. Results indicate that mitochondria tend to align tangentially to the nucleus surface, i.e., a clouds model. In addition, differences in the spatial distributions of the mitochondria were found and quantified with clearly defined metrics. The methodology here presented can be extended to other acquisition settings where the distribution and alignment of cells could be important, for instance, histopathology.

bioinformatics↗

bioRxiv2023

Relationship Between Irregularities of the Nuclear Envelope and Mitochondria in HeLa cells Observed with Electron Microscopy

This paper describes a methodology to analyse the complexity of HeLa cells as observed with electron microscopy, in particular the relationship between mitochondria and the roughness of the nuclear envelope as reflected by the invaginations of the surface. For this purpose, several segmentation mitochondria algorithms were quantitatively compared, namely: Topology, Image Processing, Topology and Image Processing, and Deep Learning, which provided the highest accuracy. The invaginations were successfully segmented with one image processing algorithm. Metrics were extracted for both structures and correlations between the mitochondria and invaginations were explored for 25 segmented cells. It was found that there was a positive correlation between the volume of invaginations and the volume of mitochondria, and negative correlations between the number and the mean volume of mitochondria, and between the volume of the cytoplasm and the aspect ratio of mitochondria. These results suggest that there is a relationship between the shape of a cell, its nucleus and its mitochondria; as well as a relationship between the number of mitochondria and their shapes. Whilst these results were obtained from a single cell line and a relatively small number of cells, they encourage further study as the methodology proposed can be easily applied to other cells and settings. Code and data are freely available. HeLa images are available from http://dx.doi.org/10.6019/EMPIAR-10094, code from https://github.com/reyesaldasoro/MitoEM, and segmented nuclei, cells, invaginations and mitochondria from https://github.com/reyesaldasoro/HeLa_Cell_Data.

bioinformatics↗

bioRxiv2021

Loss of SORCS2 is associated with neuronal DNA double-strand breaks

SORCS2 is one of five proteins that constitute the Vps10p-domain receptor family. Members of this family play important roles in cellular processes linked to neuronal survival, differentiation and function. Genetic and functional studies implicate SORCS2 in cognitive function, as well as in neurodegenerative and psychiatric disorders. DNA damage and DNA repair deficits are linked to ageing and neurodegeneration, and transient neuronal DNA double-strand breaks (DSBs) also occur as a result of neuronal activity. Here, we report a novel role for SORCS2 in DSB formation. We show that SorCS2 loss is associated with elevated DSB levels in the mouse dentate gyrus and that knocking out SORCS2 in a human neuronal cell line increased Topoisomerase II{beta}-dependent DSB formation and reduced neuronal viability. Neuronal stimulation had no impact on levels of DNA breaks in vitro, suggesting that the observed differences may not be the result of aberrant neuronal activity in these cells. Our findings are consistent with studies linking the VPS10 receptors and DNA damage to neurodegenerative conditions.

neuroscience↗