Publications by authors named "Mikael Pezet"
Article Synopsis
- CRISPRmap is a new method for optical pooled genetic screening that allows researchers to study spatial phenotypes without destroying cells, focusing on how cells respond to CRISPR modifications.
- This method integrates guide-identifying barcodes with advanced imaging techniques like immunofluorescence and RNA detection to improve the efficiency of reading the genetic information.
- In a study using breast cancer cells, CRISPRmap helped identify potentially harmful gene mutations associated with DNA damage repair, providing insights into their impact on treatment responses.
Article Synopsis
- Scientists found a new way to study how human lungs can heal themselves using special cells created from human stem cells.
- These special cells, called distal lung epithelial progenitors (DLEPs), can help repair damaged lung tissue and make important structures for lung health.
- This discovery could help researchers create new treatments for lung diseases in the future.
Article Synopsis
- Human lungs have specific cell populations in the distal respiratory airways that are linked to diseases like lung injury, COPD, and IPF, but their functions are not well understood.
- Researchers developed expandable spheres called induced respiratory airway progenitors (iRAPs) from human pluripotent stem cells, which include all cell types found in the respiratory airways.
- iRAPs can differentiate into key alveolar cell types and show defects associated with IPF when a specific gene (HPS1) is deleted, suggesting that these airway-associated cells play a role in lung regeneration and disease progression.
Heteroplasmic mitochondrial DNA (mtDNA) mutations are a common cause of inherited disease, but a few recurrent mutations account for the vast majority of new families. The reasons for this are not known. We studied heteroplasmic mice transmitting m.
View Article and Find Full Text PDFMost humans carry a mixed population of mitochondrial DNA (mtDNA heteroplasmy) affecting ~1-2% of molecules, but rapid percentage shifts occur over one generation leading to severe mitochondrial diseases. A decrease in the amount of mtDNA within the developing female germ line appears to play a role, but other sub-cellular mechanisms have been implicated. Establishing an in vitro model of early mammalian germ cell development from embryonic stem cells, here we show that the reduction of mtDNA content is modulated by oxygen and reaches a nadir immediately before germ cell specification.
View Article and Find Full Text PDFInherited mutations in the mitochondrial (mt)DNA are a major cause of human disease, with approximately 1 in 5000 people affected by one of the hundreds of identified pathogenic mtDNA point mutations or deletions. Due to the severe, and often untreatable, symptoms of many mitochondrial diseases, identifying how these mutations are inherited from one generation to the next has been an area of intense research in recent years. Despite large advances in our understanding of this complex process, many questions remain unanswered, with one of the most hotly debated being whether or not purifying selection acts against pathogenic mutations during germline development.
View Article and Find Full Text PDFThe TP53 gene plays essential roles in cancer. Conventionally, wild type (WT) p53 is thought to prevent cancer development and metastasis formation, while mutant p53 has transforming abilities. However, clinical studies failed to establish p53 mutation status as an unequivocal predictive or prognostic factor of cancer progression.
View Article and Find Full Text PDFIn vitro corticogenesis from embryonic stem cells (ESCs) is an attractive model of cortical development and a promising tool for cortical therapy. It is unknown to which extent epigenetic mechanisms crucial for cortex development and function, such as parental genomic imprinting, are recapitulated by in vitro corticogenesis. Here, using genome-wide transcriptomic and methylation analyses on hybrid mouse tissues and cells, we find a high concordance of imprinting status between in vivo and ESC-derived cortices.
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