Yi Qiu, Ph.D.

Qiu_YiAssistant Professor

Office: CGRC 356
Email: qiuy@ufl.edu
Phone: (352) 273-8201

Education and Training

Ph.D. – Mississippi State University (Animal Physiology)
M.Sc. – Chinese Academy of Science in Shanghai, China (Entomology)
B.Sc. – Peking University, China (Zoology)

Research Interests

The research interest in my lab is to study the function and regulation of histone deacetylases in hematopoiesis and other normal or abnormal developmental programs. Histone deacetylases (HDACs) are enzymes that deacetylate histone and non-histone proteins, therefore play key roles in a variety of cellular processes. We found that HDAC1 can be acetylated and lost deacetylase activity after acetylation. Acetylated HDAC can also trans-repress the deacetylase activity of HDAC2 through dimerization and therefore regulates the overall deacetylase activity of HDAC1/2 containing corepressor complexes, which play critical roles in mammalian gene transcription. For example, the HDAC1 containing NURD corepressor complex is important for erythroid differentiation. NuRD associates with fully active HDAC1 for gene repression, however, NuRD also associates with acetylated HDAC1 for activation and promote erythroid differentiation. Thus, our studies reveal a novel mechanism for regulation of corepressor function. Dynamic acetylation of HDAC1 also plays critical role in up-regulation of p53 activity in response to cellular stress. HDACs and its counterpart histone acetyltransferase (HAT) are often considered be recruited to chromatin through interaction with other chromatin interacting proteins. However, our study demonstrates that HDAC and HAT can directly interact with chromatin and they compete for chromatin binding. This finding explains why HDAC is recruited to chromatin region in a genome wide scale where no apparent chromatin binding protein is present.

There are growing numbers of studies showing increased expression of class I HDACs in human cancers. Overexpression of HDACs in cancer cells is directly linked to accelerated cell proliferation and survival. Therefore, HDAC inhibitors emerge as a class of chemotherapeutic agents for cancer treatment. However, little is known about how HDACs expression is regulated in cancer cells. We found that HDAC1 and HDAC2 promoter activity is differentially regulated by the aberrant recruitment of transcription factors and epigenetic modifiers in colon cancer cells and patient tumor samples. Meanwhile, we identified a group of small targeting molecules that specifically binds to unique dimerization domain of HDAC1 and 2, therefore block the deacetylase activity of HDAC1 and 2. Studies are in progress to examine the efficacy of these inhibitors in treating colon cancer.


Deng C, Li Y, Zhou L, Cho J, Patel B, Terada N, Li Y, Bungert J, Qiu Y* and Suming Huang*. HoxBlinc RNA recruits Set1/MLL complexes to activate Hox gene expression patterns and mesoderm lineage development. Cell Reports 14(1):103-14(2016) *co-coresponding authors

Yang H, Yan B, Liao D, Huang S, Qiu Y. Acetylation of HDAC1 and degradation of SIRT1 form a positive feedback loop to regulate p53 acetylation during heat shock stress. Cell Death & Dis. 2015 May 7;6:e1747. doi: 10.1038/cddis.2015.106. Pubmed

Tusi BK, Deng C, Salz T, Zeumer L, Li Y, So ECW, Morel LM, Qiu Y* and Huang S*. Setd1a regulates progenitor B-cell-to-precursor B-cell development through histone H3 lysine 4 trimethylation and Ig heavy-chain rearrangement. FASEB J. 29(4):1505-15 (2015) | Pubmed *co-corresponding authors

Yan B, Li X, Johnson A, Yang Y, Jian W and Qiu Y. Chapter 18: Epigenetic drugs for cancer therapy. In Epigenetic Gene Expression and Regulation. pp397-423. Suming Huang (ed.), Elsevier ISBN: 978-0-12-799958-6 (2015)

Yang H, Salz T, Zajac-Kaye M, Liao D, Huang S and Qiu Y. The overexpression of histone deacetylases in cancer cells is controlled by interplay of transcription factors and epigenetic modulators. FASEB J Jun 19, 2014. pii: fj.14-250654. [Epub ahead of print] Pubmed

Li X, Yang H, Huang S, and Qiu Y. Histone Deacetylase 1 and p300 Can Directly Associate with Chromatin and Compete for Binding in a Mutually Exclusive Manner. PLoS One 9: e94523. (2014)

Salz T., Li G., Kaye F., Zhou L., Qiu Y., and Huang S. hSETD1A regulates Wnt target genes and controls tumor growth of colorectal cancer cells. Cancer res. 74(3): 775-786. (2014) | Pubmed

Dobbin MM, Madabhushi R, Pan L, Chen Y, Kim D, Gao J, Ahanonu B, Pao PC, Qiu Y., Zhao Y, Tsai L-H. SIRT1 collaborates with ATM and HDAC1 to maintain genomic stability in neurons. Nat Neurosci, 16:1008-1015. (2013) | Pubmed

Patel B., Kang Y., Cui K., Litt M., St. Just Piberio M., Deng C., Salz T., Casada S., Fu X., Qiu Y., Zhao K., and Huang S. Aberrant TAL1 activation is mediated by an interchromosome interaction in human T-cell acute lymphoblastic leukemia. Leukemia 28(2): 349-361. (2013) | Pubmed

Deng C., Li Y., Liang S., Cui K., Salz T., Yang H., Tang Y., Gallagher PG., Qiu Y., Roeder RG., Zhao K., Bungert J., and Huang S. USF1 and hSET1A mediated epigenetic modifications regulate lineage differentiation and HoxB4 transcription. PloS. Genet. 9 (6): e1003524 (2013) | Pubmed

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Major Teaching Responsibilities

GMS 6692 Research Conference in Anatomy and Cell Biology
GMS 6421 Advanced Cell Biology
GMS 6062 Protein Trafficking
GMS 6647 Transcription Regulation
GMS 6644 Apoptosis
GMS 6061 The Nucleus