Ong Chin Tong, Ph.D.
Principal Investigator

Ong Chin Tong obtained his bachelor in Cell and Molecular Biology from the National University of Singapore (NUS). He received his Ph.D. in Developmental Biology from Washington University in St Louis where he studied Notch transcriptional regulation under Raphael Kopan. He continued his postdoctoral training with Victor Corces at Emory University where he studied the gene regulation by 3D genome organization. He joined Temasek Life Sciences Laboratory (TLL) as a Principal Investigator in Nov 2014 to study epigenetic regulation of aging and Alzheimer’s disease.


You may wish to contact Dr ONG Chin Tong at:

Tel: (65) 6872 7000, (65) 6872 7978 (DID) 

For information on PhD studies at TLL, click HERE

Research Interests

  • Epigenetic regulation of aging
  • Alzheimer’s disease

Research Projects Background and significance Alzheimer’s disease (AD) is a devastating neurodegenerative disorder characterized by long asymptomatic preclinical phase. AD remains incurable due to late detection, where toxic accumulation of amyloid plaques, neurofibrillary Tau tangles and inflammation have caused irreversible damages to the brain. It is therefore crucial to find early diagnostic markers that can reliably predict the possibility of AD occurrence before clinical manifestation of dementia.

Roles of intron retention in aging and AD pathology  Through bioinformatic analysis of model animals and AD cohorts, we found that increased intron retention is a transcriptional signature that is associated with aging and AD progression (Figure A) (Adusumalli et al., 2019). As some of mRNAs with retained introns are translated into mutated proteins, we aim to understand how they may impact aging and AD pathology.

How DNA methylation can be fine-tuned in locus-specific manner  Epigenome-wide association studies showed that changes in the DNA methylation patterns at specific AD-linked genetic loci may predict the occurrence and severity of AD. Understanding what regulates these changes may provide insights into the mechanisms that trigger AD pathology during aging. We found that the DNA demethylase activity of TET3 is regulated by phosphorylation during neurogenesis (Figure B) (Rao et al., 2020). We aim to uncover other mechanisms that regulate the level of DNA methylation at specific genetic loci in the context of aging and AD.

Epigenetic regulation of aging Aging is the major risk factor of late-onset sporadic AD. We use Drosophila as a model system to identify the epigenetic mechanisms that regulate organismal aging to uncover potential pro-longevity targets.   Figure. Elucidate mechanisms that regulate aging and AD pathology. (A) There is elevated level of intron retention (IR) during aging and in AD brain tissues. More than 15% of the 781 genes with aberrant IR shows significant differences in their protein expression level between control and AD brain tissues. PFC: Prefrontal cortex. (B) DNMT converts cytosine to repressive 5mC mark, which is further oxidized by TET enzymes into active 5hmC mark on DNA. Tet3 undergoes phosphorylation at the highly conserved SPX(K/R) motif. Cells expressing wild-type WT Tet3 activate neuronal programs whereas cells with phosphor-mutant AA Tet3 turn on metabolic pathways.