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9. FOXG1 Is Responsible for the Congenital Variant of Rett Syndrome

Author

Ariani, Francesca, Hayek, G., Rondinella, D., Artuso, R., Mencarelli, M. A., Spanhol Rosseto, A., Pollazzon, M., Buoni, S., Spiga, Ottavia, Ricciardi, S., Meloni, Ilaria, Longo, I., Mari, F., Broccoli, V., Zappella, M., Renieri, Alessandra, and Mari, Francesca

Subjects
Adult, Models, Molecular, Protein Denaturation, Protein Folding, Transcription, Genetic, Protein Conformation, Molecular Sequence Data, CDKL5, Repressor, Nerve Tissue Proteins, Rett syndrome, Biology, MECP2, Cohort Studies, Degenerative disease, Report, Rett Syndrome, Genetics, medicine, Humans, Genetics(clinical), Atypical Rett syndrome, Amino Acid Sequence, Child, Gene, In Situ Hybridization, Genetics (clinical), Brain, Forkhead Transcription Factors, medicine.disease, Repressor Proteins, FOXG1, nervous system, Mutation, Female
Abstract

Rett syndrome is a severe neurodevelopmental disease caused by mutations in the X-linked gene encoding for the methyl-CpG-binding protein MeCP2. Here, we report the identification of FOXG1-truncating mutations in two patients affected by the congenital variant of Rett syndrome. FOXG1 encodes a brain-specific transcriptional repressor that is essential for early development of the telencephalon. Molecular analysis revealed that Foxg1 might also share common molecular mechanisms with MeCP2 during neuronal development, exhibiting partially overlapping expression domain in postnatal cortex and neuronal subnuclear localization.

Published
2008

14. Differentiation of early neuroectodermal precursors derived from human embryonic stem cells into neural crest cells and dopaminergic neurone

Author

Colleoni S., Broccoli V., GALLI, CESARE, LAZZARI, GIOVANNA, Colleoni S., Broccoli V., Galli C., and Lazzari G.

Subjects
endocrine system, animal structures, neuroectodermal precursor, embryonic structures, human embryonic stem cell, neural crest cell, dopaminergic neurone
Abstract

Differentiation of early neuroectodermal precursors derived from human embryonic stem cells into neural crest cells and dopaminergic neurone

Published
2008

27. The A-Myb transcription factor is a marker of centroblasts in vivo

Author

Golay J, Broccoli V, Lamorte G, Bifulco C, Parravicini C, Arnold Pizzey, Ns, Thomas, Delia D, Ferrauti P, Vitolo D, and Introna M

Subjects
B-Lymphocytes, Immunology, Cell Cycle, Cell Differentiation, A-Myb transcription factor, B lymphocytes, germinal center differentiation, Germinal Center, Lymphocyte Activation, Proto-Oncogene Mas, Gene Expression Regulation, Proto-Oncogene Proteins, Trans-Activators, Immunology and Allergy, Humans, Biomarkers, Cell Division
Abstract

The A-Myb transcription factor is structurally related to the c-myb proto-oncogene and is involved in the control of proliferation and/or differentiation of mature B lymphocytes. We have shown previously by PCR analysis that A-myb is preferentially expressed in CD38+CD39−sIgM− mature B cells. We demonstrate here, using in situ hybridization, that A-mybexpression is restricted to the dark zone of human tonsils and lymph nodes. Furthermore, we show that A-Myb expression is cell cycle regulated both in tonsillar B cells and in Burkitt’s lymphoma cell lines, being detectable only in the S and G2/M phases of the cell cycle and not in G0/G1 phase. Strong proliferation of resting human B cells induced in vitro by a variety of physiologic signals, including anti-μ, CD40 ligand, IL-2, IL-4, IL-6, IL-13, IFN-γ, TNF-α, anti-CD19, and anti-CD20, failed to induce A-myb expression, suggesting that proliferation alone is not sufficient for A-myb expression in the absence of induction of a true centroblast phenotype. Finally, we show that differentiation of germinal center B cells in vitro toward either memory or plasma cells is accompanied by rapid down-regulation of A-myb expression. We conclude that A-myb is a marker of centroblasts generated in vivo.

Published
1998

28. 1 Body plan genes and human malformation

Author

Boncinelli, E., Mallamaci, A., and Broccoli, V.

Subjects
TERMINAL CLEAVAGE PRODUCT, Central nervous system, RENAL COLOBOMA SYNDROME, VERTEBRATE HOMEOBOX GENES
Published
1998

32. Emx and Otx gene expression in the developing mouse brain

Author

Boncinelli E, Gulisano M, Fabio Spada, and Broccoli V

Subjects
Mice, Genes, Homeobox, Animals, Brain, Gene Expression Regulation, Developmental
Abstract

The homeobox genes Emx1, Emx2, Otx1 and Otx2 are all expressed in the rostral brain of embryos at E10. Their expression domains are continuous regions of the developing brain contained within each other, such that the expression domain of Otx2 contains that of the other three genes, the expression domain of Otx1 contains that of Emx1 and Emx2, and the expression domain of Emx2 contains that of Emx1. The Emx1 expression domain includes the dorsal telencephalon and it has a posterior boundary slightly anterior to that between the presumptive diencephalon and telencephalon, whereas the Otx2 expression domain covers almost the entire forebrain and midbrain. Starting from E10.75, Otx2 expression disappears progressively from the presumptive cerebral cortex, whereas Emx1, Emx2 and Otx1 are expressed in this structure until late gestation. In particular, Emx2 appears to be expressed exclusively in the germinal ventricular zone of the developing cerebral cortex.

Published
1995

42. The homeobox gene Arx is a novel positive regulator of embryonic myogenesis.

Author

Biressi, S., Messina, G., Collombat, P., Tagliafico, E., Monteverde, S., Benedetti, L., Cusella De Angelis, M. G., Mansouri, A., Ferrari, S., Tajbakhsh, S., Broccoli, V., and Cossu, G.

Subjects
MYOGENESIS, MYOBLASTS, CELL lines, MUSCLE cells, CELL culture
Abstract

Skeletal muscle fibers form in overlapping, but distinct phases that depend on the generation of temporally different lineages of myogenic cells. During primary myogenesis (E10.5–E12.5 in the mouse), embryonic myoblasts fuse homotypically to generate primary fibers, whereas during later development (E14.5–E17.5), fetal myoblasts differentiate into secondary fibers. How these myogenic waves are regulated remains largely unknown. Studies have been hampered by the lack of markers which would distinguish embryonic from fetal myoblast populations. We show here that the homeobox gene Arx is strongly expressed in differentiating embryonic muscle, downstream of myogenic basic helix–loop–helix (bHLH) genes. Its expression progressively decreases during development. When overexpressed in the C2C12 myogenic cell line, Arx enhances differentiation. Accordingly, it stimulates the transcriptional activity from the Myogenin promoter and from multimerized E-boxes when co-expressed with MyoD and Mef2C in CH310T1/2. Furthermore, Arx co-immunoprecipitates with Mef2C, suggesting that it participates in the transcriptional regulatory network acting in embryonic muscle. Finally, embryonic myoblasts isolated from Arx-deficient embryos show a delayed differentiation in vivo together with an enhanced clonogenic capacity in vitro. We propose here that Arx acts as a novel positive regulator of embryonic myogenesis by synergizing with Mef2C and MyoD and by establishing an activating loop with Myogenin.Cell Death and Differentiation (2008) 15, 94–104; doi:10.1038/sj.cdd.4402230; published online 12 October 2007 [ABSTRACT FROM AUTHOR]

Published
2008
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48. Regulation of hematopoietic cell proliferation and differentiation by themyboncogene family of transcription factors

Author

Golay, J., Basilico, L., Loffarelli, L., Songia, S., Broccoli, V., and Introna, M.

Abstract

Themybfamily of genes include the virally encoded v-myboncogene, its normal cellular equivalent c-myband two related members called A-myband B-myb. They are all transcription factors that recognize the same DNA sequence (PyAACG/TG) and are all involved in the regulation of proliferation and differentiation in different cell types, including hematopoietic cells. C-mybis most highly expressed in hematopoietic cells and its oncogenic activation leads to transformation of these cells. Several lines of evidence have demonstrated that c-mybregulates both the proliferation and differentiation of hematopoietic cells of different lineages. The mechanisms of action of c-myband v-mybare becoming clearer, mostly through the study of the different genes that are regulated by these transcription factors and the cofactors with which c-myband v-mybco-operate. More recently the biological and biochemical functions of the B-myband A-mybgene products have been investigated. Evidence for the function of the different members of themybfamily in relation to hematopoietic proliferation and differentiation is presented, and the different roles of themybgenes are discussed.

Published
1996
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