H. Efsun Arda

Last updated
H. Efsun Arda
H. Efsun Arda.jpg
Born
Hatice Efsun Arda
NationalityTurkish
Alma mater Boğaziçi University (BS)
University of Massachusetts Medical School (PhD)
Scientific career
FieldsDevelopmental biology
systems biology
Institutions National Cancer Institute
Thesis C. Elegans Metabolic Gene Regulatory Networks  (2010)
Doctoral advisor Marian Walhout  [ Wikidata ]

Hatice Efsun Arda is a Turkish developmental and systems biologist researching cell lineages that give rise to human pancreas using single cell sequencing. She is a Stadtman principal investigator and head of the developmental genomics group at the National Cancer Institute.

Contents

Early life and education

Hatice Efsun Arda spent time with her mother, a nurse practitioner, at a hospital and in clinical laboratories. This early exposure encouraged her to study biology and medicine. Arda completed a B.S. in molecular biology and genetics at Boğaziçi University. [1]

Arda obtained a Ph.D. in systems biology from the University of Massachusetts Medical School. During her doctorate training in the laboratory of Marian Walhout  [ Wikidata ], she studied gene regulatory networks that pertain to the metabolism of the model organism, C. elegans . She uncovered a set of metabolic genes that are sensitive to the nutrient content of C. elegans bacterial diet. [2] [3]

Postdoctoral research

Interested in gene regulatory networks and developmental biology, Arda joined the laboratory of Seung K. Kim  [ Wikidata ] at Stanford University for her postdoctoral training. As a JDRF fellow, she developed cell sorting methods to purify primary pancreatic cells from children and adults, and used RNA sequencing to reveal hundreds of genes that are differentially regulated during the first 10 years of human lifespan, several of which are linked by association studies to diabetes risk. To understand how pancreatic cell type-specific gene expression programs are controlled at the genomic level, she then combined cell sorting with genomic techniques, like ATAC-Seq to delineate the regulatory chromatin landscape of human pancreatic cell types. This work revealed thousands of putative enhancer regions that explain cell type-specific gene expression in the human pancreas. [2]

In 2016, Arda's research showed that the beta cells in the human pancreas continue their maturation after birth. Arda and colleagues examined the gene expression and chromatin profiles of pancreas cells isolated from children and adults and found specific gene-expression programs that are turned on after the age of 10. The study was the first to demonstrate these differences at a global level, and the team uncovered new factors potentially mediating this process. [1] [4]

To investigate genomic regulation, Arda continued to research the DNA elements that control pancreas-cell specification, identity, and function. Arda and co-authors and generated an atlas of genomic elements specific to the main cell types in the human pancreas. She identified unique regions in our genomes that control cell-type-specific gene expression in human pancreas cells. These regions also turned out to harbor more disease-risk variants associated with diabetes or pancreas cancer than other parts of the human genome. [1] [5]

Career and research

Arda joined the National Institutes of Health in 2017 as a Stadtman principal investigator in the laboratory of receptor biology and gene expression at the National Cancer Institute. She is head of the developmental genomics group. [2]

Arda's laboratory aims to delineate the gene regulatory networks that control the development, expansion and function of human pancreatic cells. Her research group combines genomic approaches with use of primary human cells, stem cell and genome-editing technologies to build maps of regulatory genomes governing the establishment and growth of human pancreatic cell lineages. Arda characterizes the cell lineages that give rise to human pancreas using single cell sequencing. [2]

Related Research Articles

<span class="mw-page-title-main">Comparative genomics</span> Field of biological research

Comparative genomics is a branch of biological research that examines genome sequences across a spectrum of species, spanning from humans and mice to a diverse array of organisms from bacteria to chimpanzees. This large-scale holistic approach compares two or more genomes to discover the similarities and differences between the genomes and to study the biology of the individual genomes. Comparison of whole genome sequences provides a highly detailed view of how organisms are related to each other at the gene level. By comparing whole genome sequences, researchers gain insights into genetic relationships between organisms and study evolutionary changes. The major principle of comparative genomics is that common features of two organisms will often be encoded within the DNA that is evolutionarily conserved between them. Therefore, Comparative genomics provides a powerful tool for studying evolutionary changes among organisms, helping to identify genes that are conserved or common among species, as well as genes that give unique characteristics of each organism. Moreover, these studies can be performed at different levels of the genomes to obtain multiple perspectives about the organisms.

<span class="mw-page-title-main">Functional genomics</span> Field of molecular biology

Functional genomics is a field of molecular biology that attempts to describe gene functions and interactions. Functional genomics make use of the vast data generated by genomic and transcriptomic projects. Functional genomics focuses on the dynamic aspects such as gene transcription, translation, regulation of gene expression and protein–protein interactions, as opposed to the static aspects of the genomic information such as DNA sequence or structures. A key characteristic of functional genomics studies is their genome-wide approach to these questions, generally involving high-throughput methods rather than a more traditional "candidate-gene" approach.

<span class="mw-page-title-main">Epigenome</span> Biological term

In biology, the epigenome of an organism is the collection of chemical changes to its DNA and histone proteins that affects when, where, and how the DNA is expressed; these changes can be passed down to an organism's offspring via transgenerational epigenetic inheritance. Changes to the epigenome can result in changes to the structure of chromatin and changes to the function of the genome. The human epigenome, including DNA methylation and histone modification, is maintained through cell division. The epigenome is essential for normal development and cellular differentiation, enabling cells with the same genetic code to perform different functions. The human epigenome is dynamic and can be influenced by environmental factors such as diet, stress, and toxins.

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<span class="mw-page-title-main">Victor Velculescu</span>

Victor E. Velculescu is a Professor of Oncology and Co-Director of Cancer Biology at Johns Hopkins University School of Medicine. He is internationally known for his discoveries in genomics and cancer research.

Epigenomics is the study of the complete set of epigenetic modifications on the genetic material of a cell, known as the epigenome. The field is analogous to genomics and proteomics, which are the study of the genome and proteome of a cell. Epigenetic modifications are reversible modifications on a cell's DNA or histones that affect gene expression without altering the DNA sequence. Epigenomic maintenance is a continuous process and plays an important role in stability of eukaryotic genomes by taking part in crucial biological mechanisms like DNA repair. Plant flavones are said to be inhibiting epigenomic marks that cause cancers. Two of the most characterized epigenetic modifications are DNA methylation and histone modification. Epigenetic modifications play an important role in gene expression and regulation, and are involved in numerous cellular processes such as in differentiation/development and tumorigenesis. The study of epigenetics on a global level has been made possible only recently through the adaptation of genomic high-throughput assays.

<span class="mw-page-title-main">STARR-seq</span>

STARR-seq is a method to assay enhancer activity for millions of candidates from arbitrary sources of DNA. It is used to identify the sequences that act as transcriptional enhancers in a direct, quantitative, and genome-wide manner.

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H3K4me3 is an epigenetic modification to the DNA packaging protein Histone H3 that indicates tri-methylation at the 4th lysine residue of the histone H3 protein and is often involved in the regulation of gene expression. The name denotes the addition of three methyl groups (trimethylation) to the lysine 4 on the histone H3 protein.

Centre for Genomic Regulation

The Centre for Genomic Regulation is a biomedical and genomics research centre based in Barcelona. Most of its facilities and laboratories are located in the Barcelona Biomedical Research Park, in front of Somorrostro beach.

H3K9me3 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the tri-methylation at the 9th lysine residue of the histone H3 protein and is often associated with heterochromatin.

H3K4me1 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the mono-methylation at the 4th lysine residue of the histone H3 protein and often associated with gene enhancers.

H3K36me3 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the tri-methylation at the 36th lysine residue of the histone H3 protein and often associated with gene bodies.

H4K20me is an epigenetic modification to the DNA packaging protein Histone H4. It is a mark that indicates the mono-methylation at the 20th lysine residue of the histone H4 protein. This mark can be di- and tri-methylated. It is critical for genome integrity including DNA damage repair, DNA replication and chromatin compaction.

H3K23ac is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the acetylation at the 23rd lysine residue of the histone H3 protein.

H3K9ac is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the acetylation at the 9th lysine residue of the histone H3 protein.

H3K36me2 is an epigenetic modification to the DNA packaging protein Histone H3. It is a mark that indicates the di-methylation at the 36th lysine residue of the histone H3 protein.

<span class="mw-page-title-main">MNase-seq</span> Method used to analyse protein interactions with DNA

MNase-seq, short for micrococcal nuclease digestion with deep sequencing, is a molecular biological technique that was first pioneered in 2006 to measure nucleosome occupancy in the C. elegans genome, and was subsequently applied to the human genome in 2008. Though, the term ‘MNase-seq’ had not been coined until a year later, in 2009. Briefly, this technique relies on the use of the non-specific endo-exonuclease micrococcal nuclease, an enzyme derived from the bacteria Staphylococcus aureus, to bind and cleave protein-unbound regions of DNA on chromatin. DNA bound to histones or other chromatin-bound proteins may remain undigested. The uncut DNA is then purified from the proteins and sequenced through one or more of the various Next-Generation sequencing methods.

H3K36me is an epigenetic modification to the DNA packaging protein Histone H3, specifically, the mono-methylation at the 36th lysine residue of the histone H3 protein.

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References

  1. 1 2 3 Carter, Laura Stephenson (2019-12-19). "Getting to Know 11 Stadtmans". NIH Intramural Research Program. Retrieved 2020-05-05.PD-icon.svg This article incorporates text from this source, which is in the public domain .
  2. 1 2 3 4 "H. Efsun Arda, Ph.D." Center for Cancer Research. 2017-09-25. Retrieved 2020-05-05.PD-icon.svg This article incorporates text from this source, which is in the public domain .
  3. ↑ Arda, H. (2010-07-30). C. Elegans Metabolic Gene Regulatory Networks: A Dissertation. GSBS Dissertations and Theses (Thesis). University of Massachusetts Medical School. doi:10.13028/9v59-hc11.
  4. ↑ Arda, H. Efsun; Li, Lingyu; Tsai, Jennifer; Torre, Eduardo A.; Rosli, Yenny; Peiris, Heshan; Spitale, Robert C.; Dai, Chunhua; Gu, Xueying; Qu, Kun; Wang, Pei (2016). "Age-Dependent Pancreatic Gene Regulation Reveals Mechanisms Governing Human β Cell Function". Cell Metabolism. 23 (5): 909–920. doi:10.1016/j.cmet.2016.04.002. PMC   4864151 . PMID   27133132.
  5. ↑ Arda, H. Efsun; Tsai, Jennifer; Rosli, Yenny R.; Giresi, Paul; Bottino, Rita; Greenleaf, William J.; Chang, Howard Y.; Kim, Seung K. (2018). "A Chromatin Basis for Cell Lineage and Disease Risk in the Human Pancreas". Cell Systems. 7 (3): 310–322.e4. doi:10.1016/j.cels.2018.07.007. PMC   6347013 . PMID   30145115.
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