Hierarchical Structures and Dissected Functions of MADS-Box Transcription Factors in Rice Development

Author(s):  
Jinmi Yoon ◽  
Lae-Hyeon Cho ◽  
Ki-Hong Jung
1995 ◽  
Vol 229 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Paul Shore ◽  
Andrew D. Sharrocks

2013 ◽  
Vol 13 (5-6) ◽  
pp. 160-170 ◽  
Author(s):  
Jérôme Puig ◽  
Donaldo Meynard ◽  
Giang Ngan Khong ◽  
Germain Pauluzzi ◽  
Emmanuel Guiderdoni ◽  
...  

1999 ◽  
Vol 19 (4) ◽  
pp. 2853-2862 ◽  
Author(s):  
Jeanne Wilson-Rawls ◽  
Jeffery D. Molkentin ◽  
Brian L. Black ◽  
Eric N. Olson

ABSTRACT Skeletal muscle gene expression is dependent on combinatorial associations between members of the MyoD family of basic helix-loop-helix (bHLH) transcription factors and the myocyte enhancer factor 2 (MEF2) family of MADS-box transcription factors. The transmembrane receptor Notch interferes with the muscle-inducing activity of myogenic bHLH proteins, and it has been suggested that this inhibitory activity of Notch is directed at an essential cofactor that recognizes the DNA binding domains of the myogenic bHLH proteins. Given that MEF2 proteins interact with the DNA binding domains of myogenic bHLH factors to cooperatively regulate myogenesis, we investigated whether members of the MEF2 family might serve as targets for the inhibitory effects of Notch on myogenesis. We show that a constitutively activated form of Notch specifically blocks DNA binding by MEF2C, as well as its ability to cooperate with MyoD and myogenin to activate myogenesis. Responsiveness to Notch requires a 12-amino-acid region of MEF2C immediately adjacent to the DNA binding domain that is unique to this MEF2 isoform. Two-hybrid assays and coimmunoprecipitations show that this region of MEF2C interacts directly with the ankyrin repeat region of Notch. These findings reveal a novel mechanism for Notch-mediated inhibition of myogenesis and demonstrate that the Notch signaling pathway can discriminate between different members of the MEF2 family.


1997 ◽  
Vol 17 (5) ◽  
pp. 2876-2887 ◽  
Author(s):  
A G West ◽  
P Shore ◽  
A D Sharrocks

The serum response factor (SRF) and myocyte enhancer factor 2A (MEF2A) represent two human members of the MADS-box transcription factor family. Each protein has a distinct biological function which is reflected by the distinct specificities of the proteins for coregulatory protein partners and DNA-binding sites. In this study, we have investigated the mechanism of DNA binding utilized by these two related transcription factors. Although SRF and MEF2A belong to the same family and contain related DNA-binding domains, their DNA-binding mechanisms differ in several key aspects. In contrast to the dramatic DNA bending induced by SRF, MEF2A induces minimal DNA distortion. A combination of loss- and gain-of-function mutagenesis identified a single amino acid residue located at the N terminus of the recognition helices as the critical mediator of this differential DNA bending. This residue is also involved in determining DNA-binding specificity, thus indicating a link between DNA bending and DNA-binding specificity determination. Furthermore, different basic residues within the putative recognition alpha-helices are critical for DNA binding, and the role of the C-terminal extensions to the MADS box in dimerization between SRF and MEF2A also differs. These important differences in the molecular interactions of SRF and MEF2A are likely to contribute to their differing roles in the regulation of specific gene transcription.


2006 ◽  
Vol 57 (13) ◽  
pp. 3419-3431 ◽  
Author(s):  
S. Ciannamea ◽  
K. Kaufmann ◽  
M. Frau ◽  
I. A. N. Tonaco ◽  
K. Petersen ◽  
...  

2017 ◽  
Vol 176 (1) ◽  
pp. 891-909 ◽  
Author(s):  
Shan Li ◽  
Huijinlan Xu ◽  
Zheng Ju ◽  
Dongyan Cao ◽  
Hongliang Zhu ◽  
...  

2019 ◽  
Author(s):  
Lydia Gramzow ◽  
Dajana Lobbes ◽  
Sophia Walter ◽  
Nathan Innard ◽  
Günter Theißen

AbstractSome microRNAs (miRNAs) are key regulators of developmental processes, mainly by controlling the accumulation of transcripts encoding transcription factors that are important for morphogenesis. MADS-box genes encode a family of transcription factors which control diverse developmental processes in flowering plants. Here we study the convergent evolution of two MIRNA (MIR) gene families, named MIR444 and MIR824, targeting members of the same clade of MIKCC-group MADS-box genes. We show that these two MIR genes most likely originated independently in monocots (MIR444) and in Brassicales (eudicots, MIR824). We provide evidence that in both cases the future target gene was transcribed in antisense prior to the evolution of the MIR genes. Both MIR genes then likely originated by a partial inverted duplication of their target genes, resulting in natural antisense organization of the newly evolved MIR gene and its target gene at birth. We thus propose a new model for the origin of MIR genes, MEPIDAS (MicroRNA Evolution by Partial Inverted Duplication of Antisense-transcribed Sequences). MEPIDAS is a refinement of the inverted duplication hypothesis. According to MEPIDAS, a MIR gene evolves at a genomic locus at which the future target gene is also transcribed in the antisense direction. A partial inverted duplication at this locus causes the antisense transcript to fold into a stem-loop structure that is recognized by the miRNA biogenesis machinery to produce a miRNA that regulates the gene at this locus. Our analyses exemplify how to elucidate the origin of conserved miRNAs by comparative genomics and will guide future studies.


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