Sat, 26 Jul 2008 06:39:41 BST CiteULike: heliopais's Olson http://www.citeulike.org/user/heliopais/author/Olson CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/heliopais/article/2718410 <i>Developmental Cell, Vol. 6, No. 3. (March 2004), pp. 423-435.</i><br /><br />Runx2 is necessary and sufficient for osteoblast differentiation, yet its expression precedes the appearance of osteoblasts by 4 days. Here we show that Twist proteins transiently inhibit Runx2 function during skeletogenesis. Twist-1 and -2 are expressed in Runx2-expressing cells throughout the skeleton early during development, and osteoblast-specific gene expression occurs only after their expression decreases. Double heterozygotes for Twist-1 and Runx2 deletion have none of the skull abnormalities observed in Runx2+/- mice, a Twist-2 null background rescues the clavicle phenotype of Runx2+/- mice, and Twist-1 or -2 deficiency leads to premature osteoblast differentiation. Furthermore, Twist-1 overexpression inhibits osteoblast differentiation without affecting Runx2 expression. Twist proteins' antiosteogenic function is mediated by a novel domain, the Twist box, which interacts with the Runx2 DNA binding domain to inhibit its function. In vivo mutagenesis confirms the antiosteogenic function of the Twist box. Thus, relief of inhibition by Twist proteins is a mandatory event precluding osteoblast differentiation. A Twist Code Determines the Onset of Osteoblast Differentiation Peter Bialek Britt Kern Xiangli Yang Marijke Schrock Drazen Sosic Nancy Hong Hua Wu Kai Yu David Ornitz Eric Olson Monica Justice Gerard Karsenty doi:10.1016/S1534-5807(04)00058-9 Developmental Cell, Vol. 6, No. 3. (March 2004), pp. 423-435. 2008-04-25T13:17:16-00:00 2004 Developmental Cell 6 3 423 435 runx2 http://www.citeulike.org/user/heliopais/article/2479085 <i>Trends in Genetics, Vol. In Press, Corrected Proof</i><br /><br />MicroRNAs negatively regulate gene expression by promoting mRNA degradation and inhibiting mRNA translation. Recent studies have uncovered a cadre of muscle-specific microRNAs that regulate diverse aspects of muscle function, including myoblast proliferation, differentiation, contractility and stress responsiveness. These myogenic microRNAs, which are encoded by bicistronic transcripts or are nestled within introns of myosin genes, modulate muscle functions by fine-tuning gene expression patterns or acting as `on-off' switches. Muscle-specific microRNAs also participate in numerous diseases, including cardiac hypertrophy, heart failure, cardiac arrhythmias, congenital heart disease and muscular dystrophy. The myriad roles of microRNAs in muscle biology pose interesting prospects for their therapeutic manipulation in muscle disease. MicroRNAs flex their muscles Eva van Rooij Ning Liu Eric Olson doi:10.1016/j.tig.2008.01.007 Trends in Genetics, Vol. In Press, Corrected Proof 2008-03-06T15:10:04-00:00 Trends in Genetics In Press, Corrected Proof microrna review http://www.citeulike.org/user/heliopais/article/892917 <i>Science, Vol. 313, No. 5795. (29 September 2006), pp. 1922-1927.</i><br /><br />The heart, an ancient organ and the first to form and function during embryogenesis, evolved by the addition of new structures and functions to a primitive pump. Heart development is controlled by an evolutionarily conserved network of transcription factors that connect signaling pathways with genes for muscle growth, patterning, and contractility. During evolution, this ancestral gene network was expanded through gene duplication and co-option of additional networks. Mutations in components of the cardiac gene network cause congenital heart disease, the most common human birth defect. The consequences of such mutations reveal the logic of organogenesis and the evolutionary origins of morphological complexity. Gene regulatory networks in the evolution and development of the heart. EN Olson doi:10.1126/science.1132292 Science, Vol. 313, No. 5795. (29 September 2006), pp. 1922-1927. 2006-10-11T15:06:25-00:00 2006 Science 1095-9203 313 5795 1922 1927 genetic_regulatory_network heart review http://www.citeulike.org/user/heliopais/article/781401 <i>Proc Natl Acad Sci U S A, Vol. 102, No. 52. (27 December 2005), pp. 18986-18991.</i><br /><br />MicroRNAs (miRNAs) are genomically encoded small RNAs that hybridize with messenger RNAs, resulting in degradation or translational inhibition of targeted transcripts. The potential for miRNAs to regulate cell-lineage determination or differentiation from pluripotent progenitor or stem cells is unknown. Here, we show that microRNA1 (miR-1) is an ancient muscle-specific gene conserved in sequence and expression in Drosophila. Drosophila miR-1 (dmiR-1) is regulated through a serum response factor-like binding site in cardiac progenitor cells. Loss- and gain-of-function studies demonstrated a role for dmiR-1 in modulating cardiogenesis and in maintenance of muscle-gene expression. We provide in vivo evidence that dmiR-1 targets transcripts encoding the Notch ligand Delta, providing a potential mechanism for the expansion of cardiac and muscle progenitor cells and failure of progenitor cell differentiation in some dmiR-1 mutants. These findings demonstrate that dmiR-1 may "fine-tune" critical steps involved in differentiation of cardiac and somatic muscle progenitors and targets a pathway required for progenitor cell specification and asymmetric cell division. MicroRNA1 influences cardiac differentiation in Drosophila and regulates Notch signaling. C Kwon Z Han EN Olson D Srivastava doi:10.1073/pnas.0509535102 Proc Natl Acad Sci U S A, Vol. 102, No. 52. (27 December 2005), pp. 18986-18991. 2006-08-01T05:28:21-00:00 2005 Proc Natl Acad Sci U S A 0027-8424 102 52 18986 18991 microrna