The discovery of the Epigenome marked the turning point for a better understanding of the complexity of gene regulation and phenotype variation.

While the largest part of available knowledge about Epigenetic mechanisms comes from studies performed in developmental contexts, very little is known about the function of the epigenome in adult tissues, how this changes in response to environment and time.​

Far from being a rigid platform, the Epigenome controls the capacity of cells to be plastic to allow adaptation and performance in response to the natural changing of environmental conditions including metabolism, stress and aging with clear implications for the understanding of tissue homeostasis, cell reprogramming and associated diseases.

The focus of our laboratory in the newly established Epigenetics program at KAUST (keep.kaust.edu.sa) is the investigation of the mechanistic role of the Epigenome and nonconding Genome in somatic cells and in particular the role of Polycomb Group Proteins (PcG), noncoding RNA, chromatin RNAi components and repetitive mobile DNA elements in cell identity, adaptation to stress, aging and reprogramming. As model system we use human primary cells and mouse animal models, with particular emphasis on skeletal muscles, neuromuscular diseases and cell reprogramming.

For more details, please refer to our laboratory’s main webs site:  Click Here

The research focuses on following two directions:

1) Characterization of molecular mechanism: how repetitive RNA modulates circadian manner of transcriptional activity and cyclic nature of metabolome homeostasis.

2) Identification of communicating signals and characterization of their contribution in orchestrating inter-organ circadian networks.

The research is characterizing the role of TEs derived repetitive RNAs during pathological aging progression. In particular the crosstalk between repetitive RNAs and chromatin remodelers activity at the onset of the aged and senescent phenotype.

The research focuses on transposable element (TE) dynamics, particularly LINE-1 (L1), in bone. Her research aims to understand how L1 dynamics are impaired in osteoporosis, and to identify TE-based approaches that improve the anabolic potential of bone tissue.

The research is focused on the analysis of non-coding transcripts including enhancer RNAs, long non-coding RNAs, and also Transposable Elements RNAs and their effect on chromatin state and genes expression during the differentiation of healthy and dystrophic human muscle cells

The research is on system biology using bioinformatics tools. His expertise is metabolic networks.

The scope of his current research is to exploit these powerful tools to answer fundamental and broad biological questions such as cell to cell communication.

Utilizing liver organoids to study the role of repeat elements in non-alcoholic fatty liver disease (NAFLD)-associated hepatocellular carcinoma (HCC).

Modulate endogenous Long Interspersed Nuclear Elements Class1 (L1) expression in human dermal fibroblasts using CRISPR activation system to study its role during somatic cell reprogramming.

The research is focused on investigating how TE-derived RNAs dysregulation impairs cellular identity and stem cell commitment in skeletal muscle cells.

We developed a RADICL-ChIP strategy to understand the complexity of the RNA network genome-wide while shedding light on regulatory pathways of chromatin-associated factors. Utilizing the dynamics of Polycomb repressive complex 2 (PRC2-Ezh1) in stress response in postmitotic muscle cells as a model system.