Tamir Chandra

The paper shows that loss of MITF activity in zebrafish melanocyte stem cells leads to premature expansion and novel transcriptional states during embryogenesis, with stage-specific effects on regeneration.

The paper develops COMET, a method to infer clonal hematopoiesis from bulk DNA methylation data, showing it accurately detects clonal expansion and replicates known genetic associations.

This study finds that DNA methylation rates negatively scale with maximum lifespan across mammals in blood and skin.

This study models how senescence spreads between cells and finds that differences in secreted signalling molecules and timedependent paracrine signalling limit its spread.

This paper improves age prediction from RRBS data by using region-based methylation averages instead of individual CpGs, showing better performance on external datasets and low coverage data.

The paper identifies DNA methylation and proteomic markers associated with brain health through integrated methylome and phenome analyses.

The paper identifies Tfap2b as a marker for melanocyte stem cells in zebrafish, showing their multi-fate potential and role in melanocyte regeneration.

This paper develops an epigenetic clock for wild wood mice using DNA methylation data to estimate age and study ageing rates in the wild.

This study identifies DNA methylation loci associated with age-by-sex interactions in a cohort of 2,586 individuals, finding most significant loci are X-linked and linked to disease-related genes.

The paper shows that age-related clonal haemopoiesis is linked to accelerated epigenetic age.

The paper identifies two distinct pluripotency states in mouse embryonic stem cells (mESCs) based on G2M phase enrichment, showing naive and formative states marked by Esrrb expression levels.

The paper identifies Notch signalling as essential for secondary senescence, distinguishing it from primary senescence through molecular endpoints.

This study shows that partial reprogramming reduces epigenetic age in human cells but decouples it from the loss of somatic identity, suggesting a safe window for rejuvenation without teratoma risk.

The paper identifies a wound-specific notochord sheath cell subpopulation expressing Wilms Tumor 1b that forms a stopper-like structure during vertebra repair in zebrafish.