Briefly summarize the article below Using an animal model, the UAB researchers found that a lack of Sp7 interrupts the maturationof two types of specialized cells that help create teeth. Such basic knowledge about thedevelopment of teeth or bones adds to understanding of craniofacial abnormalities, which areamong the most common birth defects in humans.Transcription factors are proteins that interact with DNA to turn genes on or off. In embryos,they guide differentiation from the single fertilized egg into all cells that form the different tissuesand structures of the body. One of those complex structures is the tooth.The teeth of mammals develop during embryonic growth, though they erupt only after birth. Inresearch published in the Journal of Bone and Mineral Research, Javed, a professor in the UABSchool of Dentistry's Department of Oral and Maxillofacial Surgery, used a mouse model withmutations in both copies of the gene for Sp7.It was previously known that Sp7 is required for bone development. Embryos with a doublemutation in Sp7 completely lack mineralized bone. In humans, mutation of the Sp7 gene causesosteogenesis imperfecta, a condition that affects the development of bones and craniofacialstructures. However, the role of Sp7 in embryonic tooth development was unknown.Through study of mice lacking Sp7, Javed and colleagues found that initial tooth morphogenesiswas normal, even though the animals lacked mineralized tooth sockets. However, toothdevelopment did not continue -- the animals failed to produce normal dentin, the hard tissue thatforms the bulk of the tooth, and they failed to produce normal enamel, the super-hard matrixlayer that covers the tooth. This was due to reduced proliferation, maturation and polarization ofthe tooth-forming cells called odontoblasts and ameloblasts.Odontoblasts line up side by side inside the developing tooth to form a sheet of columnar cellsthat deposit dentin. Similarly, ameloblasts line up side by side in a sheet outside the developingtooth to lay down enamel.Without Sp7, the animals had small, misshapen teeth, and the odontoblasts and ameloblastsfailed to mature beyond the pre-odontoblast and pre-ameloblast stage, as measured byabsence of mature cell markers for those two types of cells. The odontoblasts and ameloblastswere fewer in number and showed disorganized alignments.The researchers found that Sp7 in normal mice was expressed only in the dental mesenchymaltissue that gives rise to odontoblasts; it was not expressed in the oral epithelium that gives riseto ameloblasts. Since it is known that 13 different members of the fibroblast growth factor, orFgf, family act as signaling proteins between the two different tissues -- dental mesenchymeand oral epithelium -- during murine tooth development, Javed and colleagues looked forchanges in Fgf ligands in the mice lacking Sp7.They found that the Fgf3 and Fgf8 ligands, which are abundant in normal tooth development,were remarkably absent in incisor and molar teeth of the animals lacking Sp7. This indicatedthat a disrupted cross-signaling between mesenchyme and epithelium was the reason for thefailed maturation of ameloblasts. Furthermore, they found that the Sp7 transcription factordirectly controlled gene expression of the Fgf ligands.Altogether, the UAB researchers concluded that Sp7 is obligatory for differentiation ofameloblasts and odontoblasts, but not for the initial tooth morphogenesis.Co-authors with Javed on the paper, "Specificity protein 7 is required for proliferation anddifferentiation of ameloblasts and odontoblasts," are co-first authors Ji-Myung Bae and John C.Clarke, and Harunur Rashid, Mitra D. Adhami, Kayla McCullough, Jordan S. Scott and HaiyanChen, Department of Oral and Maxillofacial Surgery, UAB School of Dentistry; and Krishna M.Sinha and Benoit de Crombrugghe, M.D. Anderson Cancer Center, the University of Texas.

Question

Briefly summarize the article below Using an animal model, the UAB researchers found that a lack of Sp7 interrupts the maturationof two types of specialized cells that help create teeth. Such basic knowledge about thedevelopment of teeth or bones adds to understanding of craniofacial abnormalities, which areamong the most common birth defects in humans.Transcription factors are proteins that interact with DNA to turn genes on or off. In embryos,they guide differentiation from the single fertilized egg into all cells that form the different tissuesand structures of the body. One of those complex structures is the tooth.The teeth of mammals develop during embryonic growth, though they erupt only after birth. Inresearch published in the Journal of Bone and Mineral Research, Javed, a professor in the UABSchool of Dentistry's Department of Oral and Maxillofacial Surgery, used a mouse model withmutations in both copies of the gene for Sp7.It was previously known that Sp7 is required for bone development. Embryos with a doublemutation in Sp7 completely lack mineralized bone. In humans, mutation of the Sp7 gene causesosteogenesis imperfecta, a condition that affects the development of bones and craniofacialstructures. However, the role of Sp7 in embryonic tooth development was unknown.Through study of mice lacking Sp7, Javed and colleagues found that initial tooth morphogenesiswas normal, even though the animals lacked mineralized tooth sockets. However, toothdevelopment did not continue -- the animals failed to produce normal dentin, the hard tissue thatforms the bulk of the tooth, and they failed to produce normal enamel, the super-hard matrixlayer that covers the tooth. This was due to reduced proliferation, maturation and polarization ofthe tooth-forming cells called odontoblasts and ameloblasts.Odontoblasts line up side by side inside the developing tooth to form a sheet of columnar cellsthat deposit dentin. Similarly, ameloblasts line up side by side in a sheet outside the developingtooth to lay down enamel.Without Sp7, the animals had small, misshapen teeth, and the odontoblasts and ameloblastsfailed to mature beyond the pre-odontoblast and pre-ameloblast stage, as measured byabsence of mature cell markers for those two types of cells. The odontoblasts and ameloblastswere fewer in number and showed disorganized alignments.The researchers found that Sp7 in normal mice was expressed only in the dental mesenchymaltissue that gives rise to odontoblasts; it was not expressed in the oral epithelium that gives riseto ameloblasts. Since it is known that 13 different members of the fibroblast growth factor, orFgf, family act as signaling proteins between the two different tissues -- dental mesenchymeand oral epithelium -- during murine tooth development, Javed and colleagues looked forchanges in Fgf ligands in the mice lacking Sp7.They found that the Fgf3 and Fgf8 ligands, which are abundant in normal tooth development,were remarkably absent in incisor and molar teeth of the animals lacking Sp7. This indicatedthat a disrupted cross-signaling between mesenchyme and epithelium was the reason for thefailed maturation of ameloblasts. Furthermore, they found that the Sp7 transcription factordirectly controlled gene expression of the Fgf ligands.Altogether, the UAB researchers concluded that Sp7 is obligatory for differentiation ofameloblasts and odontoblasts, but not for the initial tooth morphogenesis.Co-authors with Javed on the paper, &#34;Specificity protein 7 is required for proliferation anddifferentiation of ameloblasts and odontoblasts,&#34; are co-first authors Ji-Myung Bae and John C.Clarke, and Harunur Rashid, Mitra D. Adhami, Kayla McCullough, Jordan S. Scott and HaiyanChen, Department of Oral and Maxillofacial Surgery, UAB School of Dentistry; and Krishna M.Sinha and Benoit de Crombrugghe, M.D. Anderson Cancer Center, the University of Texas.

Accepted Answer

Specificity protein 7 is required for proliferation and differentiation of ameloblasts and…