廈門大學(xué)生物學(xué)系導(dǎo)師：丁鳳 正文

　　姓名：丁鳳
　　性別：女　　
　　職稱：副教授　
　　學(xué)院：生命科學(xué)學(xué)院
　　研究方向：分子遺傳學(xué)
　　Email: dingf@xmu.edu.cn

　　個人簡歷：
　　1993年獲得清華大學(xué)生物科學(xué)與技術(shù)系學(xué)士學(xué)位。
　　1998年獲得 美國匹茲堡大學(xué)生物科學(xué)系, HHMI , 博士學(xué)位。
　　1998～2002 美國匹茲堡大學(xué) 博士后， 2000-2002 兼職匹茲堡大學(xué)轉(zhuǎn)基因小鼠實驗中心技術(shù)總管。
　　2002-2008 美國斯坦福大學(xué)醫(yī)學(xué)院遺傳學(xué)系 博士后。
　　2009- 廈門大學(xué)生命科學(xué)學(xué)院 副教授。

　　1993 B.S., Tsinghua University. 1998 Ph.D., University of Pittsburgh, department of Biological Science and Howard Hughes Medical Institute. 1998-2002, postdoctoral fellow, University of Pittsburgh. 2000-2002 Technical director of Transgenic and Knock out mouse facility, University of Pittsburgh. 2002-2008 Postdoctoral fellow, Stanford University, School of Medicine, Department of Genetics. 2009- Associate professor, Xiamen University, School of Life Sciences.

　　主要研究方向 （Research area）
　　利用小鼠模型和生化方法來研究人類的疾病，并且籍此探究激素的調(diào)控、食欲和代謝的調(diào)節(jié)、基因銘記的機(jī)理（genomic imprinting）, 以及非蛋白編碼（non-coding）RNA的功能。研究的重點是Prader-Willi Syndrome (PWS), 這是最常見的因遺傳而引起的肥胖癥。
非蛋白編碼RNA Snord116 基因敲掉（Knock-out）小鼠是PWS的模型，我們發(fā)現(xiàn)它們呈現(xiàn)有嚴(yán)重的生長發(fā)育遲緩，運(yùn)動技能的學(xué)習(xí)障礙，以及過度進(jìn)食等癥狀, 并且，和PWS病人一樣， Snord116-deletion 小鼠血液中有高濃度的“饑餓激素” ghrelin。

　　研究重點：
　　1．探究Snord116-deletion 小鼠過度進(jìn)食的根源，及調(diào)控正常進(jìn)食行為的機(jī)制.
　?。?） 通過阻斷ghrelin信號通路，探索貪食癥的治療方法。
　　（2）建立熒光蛋白GFP標(biāo)記系統(tǒng)來研究ghrelin 的合成與分泌的調(diào)控機(jī)制. 并以這一系統(tǒng)為平臺，篩選調(diào)節(jié)激素分泌和調(diào)控食欲的新型藥物。
　　2．利用生化方法，研究和Snord116形成絡(luò)合物的未知RNA 和蛋白質(zhì)。進(jìn)一步研究這些對生長發(fā)育和進(jìn)食行為的調(diào)控。
　　3． 利用iRNA library，系統(tǒng)性地篩查并發(fā)現(xiàn)調(diào)控PWS區(qū)域epigenetic silencing的關(guān)鍵因子.

　　Research Area:
　　We use mouse models and biochemical methods to study human genetic disease, and to gain insight into the regulatory mechanisms of gastrointestinal hormone secretion, appetite and metabolism control，and to develop effective therapeutic interventions for obesity and eating disorders.
Prader-Willi Syndrome (PWS) is the leading genetic cause of obesity. Non-coding RNA Snord116 deletion mouse model of PWS exhibits growth retardation, motor learning deficiency, hyperphagia, as well as greatly increased secretion of appetite-promoting peptide, ghrelin,
　　
　　Future research will focus on:
　　1. Study of ghrelin signaling pathway, and the development of GFP knock-in mice to investigate the control mechanism of ghrelin synthesis and secretion, as well as the abnormalities in PWS mouse models. We’ll utilize this platform to screen for potential drugs that regulate hormone production and appetite.
　　2. Biochemical study of the function of non-coding RNA Snord116．
　　3. Systematic screen for essential factors for epigenetic silencing of imprinted genes at PWS loci by RNAi technology.

　　Research Articles
　　Ding F, Li HH, Li J, Myers RM, Francke U. Neonatal Starvation Response and Developmental Changes in Gene Expression Revealed by Hypothalamic Gene Expression Profiling in Mice (Submitted)
　　Li H-H, Roy M, Kuscuoglu U, Spencer CM, Halm B, Harrison KC, Bayle JH, Splendore A, Ding F, Meltzer LA, Wright E，, Paylor R， Deisseroth K, Francke U. Induced Chromosome Deletions Cause 　　Hypersociability and Other Features of Williams-Beuren Syndrome in Mice (In press, EMBO Molecular Medicine)
　　Ding F, Li HH, Zhang S, Solomon NM, Camper SA, Francke U. SnoRNA Snord116 (Pwcr1/MBII-85) deletion causes growth retardation, motor learning deficiency, hyperphagia and elevated ghrelin levels in mouse model for Prader-Willi syndrome. PLoS ONE. 2008 Mar 5;3(3):e1709
　　Press release: http://med.stanford.edu/news_releases/2008/march/prader-willi.html
Cirio MC, Ratnam S, Ding F, Reinhart B, Navara C, Chaillet JR. Preimplantation
expression of the somatic form of Dnmt1 suggests a role in the inheritance of genomic imprinting. BMC Developmental Biology 2008, 8:9
　　Ding F, Prints Y, Dhar MS, Johnson DK, Garnacho-Montero C, Nicholls RD, Francke U. Lack of Pwcr1/MBII-85 snoRNA is critical for neonatal lethality in Prader-Willi syndrome mouse models. Mamm Genome. 2005 Jun;16(6):424-31.
　　Ding F, Patel C, Ratnam S, McCarrey JR, Chaillet JR. Conservation of Dnmt1o cytosine methyltransferase in the marsupial Monodelphis domestica. Genesis. 2003 Aug;36(4):209-13.
　　Ding F, Chaillet JR. In vivo stabilization of the Dnmt1 (cytosine-5)-methyltransferase protein. Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):14861-6.
　　Ratnam S, Mertineit C, Ding F, Howell CY, Clarke HJ, Bestor TH, Chaillet JR, Trasler JM. Dynamics of Dnmt1 methyltransferase expression and intracellular localization during oogenesis and 　　preimplantation development. Dev Biol. 2002 May 15;245(2):304-14.
　　Howell CY, Bestor TH, Ding F, Latham KE, Mertineit C, Trasler JM, Chaillet JR.Genomic imprinting disrupted by a maternal effect mutation in the Dnmt1 gene.Cell. 2001 Mar 23;104(6):829-38.
　　Ding F and Grabowski PJ, Identification of a protein component of a mammalian tRNASec complex implicated in the decoding fo UGA as selenocysteine, RNA, 1999, 5, 1561-1569
　　Ding F, Hagan JP, Wang Z, and Grabowski PJ, Biochemical properties of a novel U2AF65 protein isoform generated by alternative RNA splicing, Biochemical and Biophysical Research Communications, 1996, 224, 675-683.
　　Gong Y, Ding F, Li F, and Zhao N, Phospholipase C induced membrane fusion, Acta Biophysica Sinica, 1996, 12, (1), 43-50.

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