Biochemical and cellular discovery of microtubule-binding protein DCAMKL1 regulates osteoblast function
The International Medical Journal The Journal of Experimental Medicine published online a research paper titled Microtubule-Associated Protein DCAMKL1 regulates osteoblast function via repression of Runx2 by Shanghai Research Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences. This study found that the microtubule-binding protein DCAMKL1 regulates the function of osteoblasts by inhibiting the transcription factor RUNX2 activity.
Bone growth and metabolism are important life activities of the body. Osteoblasts are derived from mesoderm mesenchymal stem cells and can secrete and mineralize the bone matrix, thereby forming new bone structures. In this study, the lentiviral-based shRNA library was introduced into primary cultured mesenchymal stem cells, and then induced to differentiate into osteoblasts. By quantitatively detecting the activity of early differentiation marker alkaline phosphatase, high-throughput screening A new regulator of osteoblast differentiation. The study found that after the microtubule binding protein DCAMKL1 was knocked down, the differentiation ability of mesenchymal stem cells into osteoblasts increased. Dcamkl1 knockout mice have increased osteoblast function, increased bone formation rate, and increased bone density. Studies on molecular mechanisms indicate that DCAMKL1 can inhibit the activity of RUNX2, a major transcription factor for osteoblast differentiation, by increasing tubulin polymerization. Various mutations in RUNX2 lead to human autosomal dominant disease-Cleidocranial Dysplasia (CCD), which is characterized by clavicle hypoplasia and persistent skull suture opening. Consistent with this, the Runx2 heterozygous mice also showed hypoplasia of the clavicle and skull, and all of these CCD-related phenotypes were able to obtain partial responses by knocking out Dcamkl1, further confirming the genetic link between DCAMKL1 and RUNX2.
This study established the method of using forward genetics methods to screen new regulatory factors in osteoblasts, and identified a new regulatory factor that regulates the function of osteoblasts, suggesting that it may be enhanced by regulating the polymerization of microtubules. Bone strength, thereby treating diseases such as osteoporosis.
The work started with the work of researchers Zou Weiguo abroad, and was jointly completed by researchers from the Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Harvard Medical School, Cornell University, Harvard School of Stomatology, and Merck. Researcher Zou Weiguo is the first author and corresponding author of the article.
The work was supported by start-up funds from the Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, funding from the State Key Laboratory of Cell Biology, and the NIH project.
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