PEK Jun Wei received his B.Sc. (Hons) (2008) and Ph.D. (2011) from the National University of Singapore (NUS). He did his graduate research in the laboratory of Dr. Toshie Kai at the Temasek Life Sciences Laboratory (TLL) where he studied the roles of nuage and small RNAs in the Drosophila germline. In 2012, he joined the laboratories of Drs. Joseph Gall and Allan Spradling at the Carnegie Institution for Science (Department of Embryology) as a Carnegie Collaborative Fellow. He developed a research program to study a novel class of noncoding RNAs (stable intronic sequence RNAs or sisRNAs) in Drosophila. He was later named a Howard Hughes Medical Institute (HHMI) Fellow of the Life Sciences Research Foundation and awarded a fellowship from the Jane Coffin Childs Memorial Fund. He returned to TLL as a Young Investigator in November 2014 to start his independent research group.
You may wish to contact Dr PEK Jun Wei at:Tel: (65) 6872 7000, (65) 6872 7818 (DID) Email: firstname.lastname@example.org
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- Stable intronic sequence RNAs (sisRNAs): novel functions and biogenesis pathways.
Noncoding RNAs (ncRNAs) have emerged as potent agents for gene regulation during normal development and in diseases such as cancer. Since the discovery of introns in 1977, the biological significance of intronic transcripts has not been well-understood. Introns are widely considered as junk sequences interspersed between coding exons in most genes of higher eukaryotes and viruses. After transcription, intronic transcripts are spliced from the pre-mRNAs, and remain in the nucleus, where they are rapidly degraded. However, a few examples of stable intronic sequences are known, such as the small nucleolar RNAs (snoRNAs), small Cajal body specific RNAs (scaRNAs) and some microRNAs, and they function in guiding modifications of ribosomal RNAs (rRNAs) and small nuclear RNAs (snRNAs) or regulating gene expression.
Over the past 3 decades, several stable intronic sequence RNAs (sisRNAs) had been identified without clear biological functions (Pek and Okamura, 2015). Recent studies have identified various forms of sisRNAs (linear and circular) and have implicated sisRNAs in several cellular processes such as the regulation of splicing, transcription, and class switch recombination in mammalian cells (Figure 1). On a broader perspective, studying sisRNAs may provide insights to the functions and evolution of introns in eukaryotes.
Our laboratory uses Drosophila melanogaster as a model system to study the biogenesis and functions of sisRNAs. Drosophila offers an excellent model to study sisRNAs in a genetically tractable multicellular organism.
We have recently shown that sisRNAs exist in Drosophila and characterized the first sisRNA (sisR-1) (Pek et al., 2015). sisR-1 is processed from the rga pre-mRNA and processed into a nuclear form that is predicted to fold into a secondary structure that exposes a ~29 nt 3' end (Figure 2). During early embryogenesis, an antisense long ncRNA (ASTR) is transcribe from the same rga locus. ASTR promotes the expression of rga pre-mRNA during early embryogenesis. Towards late embryogenesis, sisR-1 levels start to accumulate to a level that represses the expression of ASTR, possibly via complementary base-pairing at the exposed 3' end. The down-regulation of ASTR by sisR-1 then leads to a drop in rga expression. Our study provides evidence for a sisRNA in regulating a negative feedback loop by modulating a long ncRNA (Figure 3) (Pek et al., 2015).
We are continuing to identify sisRNAs in various tissues and cell types, and study their functions in various cellular processes during development and in adults. We are also dissecting the molecular functions of sisRNAs and subsequently applying the knowledge to develop tools for genetic manipulation. To better understand the evolution of sisRNAs and their relevance to human biology, we will like to extend our analysis of sisRNAs to other model organisms and diseased models.
Legends:Figure 1. Biogenesis and functions of sisRNAs. Figure 2. Predicted secondary structure of sisR-1. Figure 3. Proposed model of a sisR-1-mediated regulatory feedback loop.