Runx2-interacting genes identified by yeast two-hybrid screening of libraries generated from hypertrophic chondrocytes.

Runx2, a member of the Runt domain family, is a well-known master transcription factor for osteoblast differentiation. Runx2 has also been shown to play essential roles during chondrocyte hypertrophy, an important late stage of endochondral ossification linking both bone and cartilage development. To identify the co-factors that may interact with Runx2 together to regulate this critical process, we have performed yeast two-hybrid (Y2H) screening using Runx2 as a bait to screen a cDNA library of hypertrophic chondrocytes. The bait expressing cassette was constructed by fusing Runx2 with the pGBKT7 vector containing the Gal4 DNA binding domain (BD). The Mate & Plate libraries were constructed using pGADT7-Rec and cDNAs derived from hypertrophic chondrocytes enriched limb tissues or hypertrophic MCT cells. After co-transformation of pGBKT7-Runx2 and the cDNA libraries, colonies that grew in nutrition deficient medium were selected and subjected to PCR and sequencing analysis. We successfully identified more than 30 candidate genes, including Lectin-1 (Lgals1), Col1a2, Edf1 and Timp-2. We have performed literature review and bioinformatics analysis of these genes using GenePaint. Most of them show ubiquitous expression with Lgals1 show enhanced expression in hypertrophic chondrocytes. We further performed preliminary expression analysis by quantitative PCR and detected differential expression of these candidate genes in proliferative and hypertrophic MCT cells, with Timp-2 significantly (around 3-fold) and Lgals1 moderately (around 1.5 fold) upregulated in hypertrophic MCT cells. Our results suggest that, candidate gene Timp-2 is very likely to interact with Runx2 and together to play essential function during cartilage development, and possibly its homeostasis.

[1]  D. Chan,et al.  Fate of growth plate hypertrophic chondrocytes: Death or lineage extension? , 2015, Development, growth & differentiation.

[2]  Liu Yang,et al.  Hypertrophic chondrocytes can become osteoblasts and osteocytes in endochondral bone formation , 2014, Proceedings of the National Academy of Sciences.

[3]  A. Poole,et al.  Changes in Gene Expression Associated with Matrix Turnover, Chondrocyte Proliferation and Hypertrophy in the Bovine Growth Plate , 2014, Acta naturae.

[4]  T. Sheu,et al.  TIMP2 deficient mice develop accelerated osteoarthritis via promotion of angiogenesis upon destabilization of the medial meniscus. , 2012, Biochemical and biophysical research communications.

[5]  S. Park,et al.  Identification of Proteins That Interact with Podocin Using the Yeast 2-Hybrid System , 2009, Yonsei medical journal.

[6]  P. Day,et al.  Cartilage gene expression correlates with radiographic severity of canine elbow osteoarthritis. , 2009, Veterinary journal.

[7]  A. Vetere,et al.  Galectin-1 in cartilage: expression, influence on chondrocyte growth and interaction with ECM components. , 2008, Matrix biology : journal of the International Society for Matrix Biology.

[8]  D. Galson,et al.  General Transcription Factor IIA-γ Increases Osteoblast-specific Osteocalcin Gene Expression via Activating Transcription Factor 4 and Runt-related Transcription Factor 2* , 2008, Journal of Biological Chemistry.

[9]  V. Geoffroy,et al.  Overexpression of the transcriptional factor Runx2 in osteoblasts abolishes the anabolic effect of parathyroid hormone in vivo. , 2007, The American journal of pathology.

[10]  Kozo Nakamura,et al.  Contribution of runt-related transcription factor 2 to the pathogenesis of osteoarthritis in mice after induction of knee joint instability. , 2006, Arthritis and rheumatism.

[11]  Brendan H. Lee,et al.  Dysregulation of chondrogenesis in human cleidocranial dysplasia. , 2005, American journal of human genetics.

[12]  Brendan H. Lee,et al.  Type X collagen gene regulation by Runx2 contributes directly to its hypertrophic chondrocyte–specific expression in vivo , 2003, The Journal of cell biology.

[13]  A. Boyde,et al.  High Bone Resorption in Adult Aging Transgenic Mice Overexpressing Cbfa1/Runx2 in Cells of the Osteoblastic Lineage , 2002, Molecular and Cellular Biology.

[14]  M. Pfaffl,et al.  A new mathematical model for relative quantification in real-time RT-PCR. , 2001, Nucleic acids research.

[15]  S. Mundlos,et al.  Regulation of chondrocyte differentiation by Cbfa1 , 1999, Mechanisms of Development.

[16]  A. Baldini,et al.  Missense mutations abolishing DNA binding of the osteoblast-specific transcription factor OSF2/CBFA1 in cleidocranial dysplasia , 1997, Nature Genetics.

[17]  Makoto Sato,et al.  Targeted Disruption of Cbfa1 Results in a Complete Lack of Bone Formation owing to Maturational Arrest of Osteoblasts , 1997, Cell.

[18]  V. Lefebvre,et al.  Type X collagen gene expression in mouse chondrocytes immortalized by a temperature-sensitive simian virus 40 large tumor antigen , 1995, The Journal of cell biology.

[19]  I. Shapiro,et al.  Hypertrophic Chondrocytes , 1990, Annals of the New York Academy of Sciences.

[20]  Toshihisa Komori,et al.  Regulation of bone development and extracellular matrix protein genes by RUNX2 , 2009, Cell and Tissue Research.

[21]  T. Komori Regulation of bone development and maintenance by Runx2. , 2008, Frontiers in bioscience : a journal and virtual library.

[22]  Gregor Eichele,et al.  GenePaint.org: an atlas of gene expression patterns in the mouse embryo , 2004, Nucleic Acids Res..

[23]  稲田 正彦 Maturational disturbance of chondrocytes in Cbfa1-deficient mice , 2000 .

[24]  W. Stetler-Stevenson,et al.  Tissue inhibitor of metalloproteinase-2 (TIMP-2) mRNA is constitutively expressed in bovine, human normal, and osteoarthritic articular chondrocytes. , 1996, Journal of cellular biochemistry.