Marta Artal‐Sanz

The paper shows that loss of MRG-1 activates a mitochondrial stress response, which contributes to nuclear changes and adaptation to mitochondrial stress rather than just heterochromatin organization.

This study shows that loss of mitochondrial glutathione reductase and thioredoxin reductase in C. elegans causes growth, fertility, and muscle defects, activates a constitutive UPRmt, and alters mitochondrial morphology.

This study shows that loss of SIN-3 in C. elegans disrupts mitochondrial function and metabolism, leading to mitochondrial fragmentation and altered metabolic flux.

The paper identifies tissue-specific chromatin binding patterns of HPL-1 and HPL-2 in C. elegans, revealing their distinct roles in gene regulation and heterochromatin maintenance.

This study shows that inactivating steroid sulfatase in C. elegans extends lifespan and reduces age-related diseases, suggesting potential therapeutic applications for aging.

This study shows that social chemical communication via trehalose and DAF-16 activation enhances recovery from L1 arrest in C. elegans.

This study shows prolonged quiescence in C. elegans L1 larvae delays cell division and is regulated by insulin signaling, with maternal age affecting recovery variability.

This study identifies ADSL's role in purine recycling pathway in C. elegans, linking it to developmental timing, germline maintenance, and muscle integrity.

The paper develops a method to analyze essential genes in C. elegans by combining flow cytometry and high-throughput image analysis to sort and study homozygous lethal mutants.