Sun Sun


Department of Chemistry & Biochemistry
The University of Texas at Austin
1 University Station A5300
Austin, TX 78712-0165





















Contact Information


Office: MBB: 3.422C
Phone: 471-5583

Lab


Office:
Phone:
Fax:

Y. Whitney Yin


Whitney.Yin@mail.utexas.edu
Assistant Professor, Faculty


Research Group


Yin Group

Education


MD, Tianjin Medical College, China, 1988
Ph.D, The University of North Carolina at Chapel Hill, 1996

Postdoctorial fellow 1998-2001; Yale University

Affiliations


Institute for Cellular and Molecular Biology;

Lab Research


Our understanding of mitochondria is changing. Discovery of mitochondrial dysfunction in several multi-system, degenerative disorders starting in 1962, completion of the genome sequence of human mitochondrial DNA (mtDNA) in 1980, and, most recently, realization that regulated changes to mitochondrial permeability, not nuclear function, are responsible for apoptosis have all created a renewed interest in the biology and clinical relevance of mitochondria.

We are interested in functional and structural studies of human mitochondrial transcription. Specifically,

Mitochondrial gene transcription initiation

Gene expression in human mitochondria reflects its endosymbiotic evolutionary heritage and comprises elements from viral, bacterial and eukaryotic systems. Transcription requires nuclear encoded gene products for a bacteriophage-like RNA polymerase (mtRNAP), three transcription factors, TFAM, TFB1M and/or TFB2M, as well as one of the two mitochondria DNA promoters, light strand promoter (LSP) or heavy strand promoter (HSP) for efficient and accurate transcription. The mitochondrial RNA polymerase, although viral in origin, is inhibited by bacterial RNA polymerase inhibitors, such as rifampin, which block the initiaition of transcription. On the other hand, mtRNAP can be directly and indirectly modified by the triiodothyronine-binding thyroid hormone nuclear receptor, c-Erb Aa1, in organello, much like its cytoplasmic,eukaryotic counterpart, RNA polymerase II. Hormonal control of gene expression, in this case relating thyroid activity to mitochondrial control of oxygen consumption, ATP synthesis and thermogenesis, is a feature unique to multicellular eukaryotes.

We would like to understand:


  • How does mtRNAP recognize its two distinct promoters? What is the control mechanism for the bi-directional transcription in mitochondria?
  • How does human thyroid hormones regulate mitochondrial gene expression?
  • How does a bacteriophage-like mitochondrial RNA polymerase evolve to be regulated by the transcription factors?


Representative Publications



Rataileau, P, Huang, X, Yin, Y. W, Vachette, P, Vonrhein .C, Bricogne, G, Roversi, P, Ilyin, V, Carter, C.W jr. "2.2 A crystal structure of tryptophanyl-tRNA syntehtase complexed with ATP in a closed, pre-transition-state conformation" JMB 325(1) (2003): 39-63.

Yin, Y. W. and Steitz, T. A "Structural basis for the transition from initiation to elongation transcription in T7 RNA polymerase" Science 298(5597) (2002): 1387-95.

Steitz. T. A. and Yin, Y. W. "Accuracy, lesion bypass, strand displacement and translocation by DNA polymerase" Proc. Royal Society. (): .