Rossella Maione

Sapienza University of Rome

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Paolo Amati

Istituto Pasteur

Cecilia Battistelli

Istituto Pasteur

Marianna Nicoletta Rossi

Roma Tre University

Mariarosaria Carbone

Istituto Pasteur

Gian María Fimia

Sapienza University of Rome

Rocco Figliola

Sapienza University of Rome

Claudio Passananti

Institute of Molecular Biology and Pathology

Vanesa Gottifredi

Fundación Instituto Leloir

Oriella Andresini

Sapienza University of Rome

Anna Busanello

Fondazione G.B. Bietti

Cooperative Institutions

Sapienza University of Rome

Istituto Pasteur

Istituti di Ricovero e Cura a Carattere Scientifico

Institute of Cell Biology and Neurobiology

University of Rome Tor Vergata

Institute of Molecular Biology and Pathology

New York University

National Research Council

Fondazione Santa Lucia

Institute of Neurobiology and Molecular Medicine

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Interdependence between muscle differentiation and cell-cycle control

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer (1997)

Rossella Maione Paolo Amati

Proteostasis

Heat shock factor

HSPA12A

10.1016/s0304-419x(96)00036-4

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Citations (56)

Mutations in the VP1 coding region of polyomavirus determine differentiating stage specificity

Journal of Virology (1992)

Laura Ricci Rossella Maione Claudio Passananti Armando Felsani Paolo Amati

Polyomavirus mutants capable of replicating in undifferentiated murine C2 myoblasts were selected and characterized. These mutants grow normally in 3T6 mouse fibroblast cells, and they do not complement the wild-type virus in coinfection experiments of C2 myoblasts. Of 12 isolates, 10 possess duplications of the regulatory region including the enhancer A domain. On the bases of the regulatory region structure and the presence and length of the enhancer duplication, the mutant viruses could be grouped into three classes. One mutant class (e.g., PyMB3) possesses an enhancer duplication of 91 bp identical to that of a previously characterized polyomavirus mutant, PyNB11/1. We have demonstrated that this enhancer duplication gives rise at its junction to a novel recognition motif for the transcriptional factor NF-1 (M. Caruso, C. Iacobini, C. Passananti, A. Felsani, and P. Amati, EMBO J. 9:947-955, 1990). The regulatory region PyMB3 virus recombined in a wild-type genome context maintains the mutant phenotype. The other two types of mutants, one with a 30-bp enhancer duplication (e.g., PyMB40) and one with a wild-type enhancer structure (e.g., PyMB27), possess two similar but distinct 6-bp deletions in the same region of the VP1 coding gene. In both cases, the ability to replicate in undifferentiated C2 myoblasts is strictly correlated to the mutation in the VP1 coding region.

Coding region

10.1128/jvi.66.12.7153-7158.1992

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p57Kip2 is Induced by MyoD Through a p73-dependent Pathway

Journal of Molecular Biology (2005)

Giovanna Vaccarello Rocco Figliola Sabrina Cramerotti Fabiana Novelli Rossella Maione

PITX2

MyoD Protein

10.1016/j.jmb.2005.12.024

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Citations (43)

A Natural Hepatocyte Growth Factor/Scatter Factor Autocrine Loop in Myoblast Cells and the Effect of the Constitutive Met Kinase Activation on Myogenic Differentiation

The Journal of Cell Biology (1997)

Sergio Anastasi Silvia Giordano Olga Sthandier Giovanna Gambarotta Rossella Maione

As a rule, hepatocyte growth factor/scatter factor (HGF/SF) is produced by mesenchymal cells, while its receptor, the tyrosine kinase encoded by the met proto-oncogene, is expressed by the neighboring epithelial cells in a canonical paracrine fashion. In the present work we show that both HGF/SF and met are coexpressed by undifferentiated C2 mouse myoblasts. In growing cells, the autocrine loop is active as the receptor exhibits a constitutive phosphorylation on tyrosine that can be abrogated by exogenously added anti-HGF/SF neutralizing antibodies. The transcription of HGF/SF and met genes is downregulated when myoblasts stop proliferating and differentiate. The coexpression of HGF/SF and met genes is not exclusive to C2 cells since it has been assessed also in other myogenic cell lines and in mouse primary satellite cells, suggesting that HGF/SF could play a role in muscle development through an autocrine way. To analyze the biological effects of HGF/SF receptor activation, we stably expressed the constitutively activated receptor catalytic domain (p65tpr-met) in C2 cells. This active kinase determined profound changes in cell shape and inhibited myogenesis at both morphological and biochemical levels. Notably, a complete absence of muscle regulatory markers such as MyoD and myogenin was observed in p65tpr-met highly expressing C2 clones. We also studied the effects of the ectopic expression of human isoforms of met receptor (h-met) and of HGF/SF (h-HGF/SF) in stable transfected C2 cells. Single constitutive expression of h-met or h-HGF/SF does not alter substantially the growth and differentiation properties of the myoblast cells, probably because of a species-specific ligand–receptor interaction. A C2 clone expressing simultaneously both h-met and h-HGF/SF is able to grow in soft agar and shows a decrease in myogenic potential comparable to that promoted by p65tpr-met kinase. These data indicate that a met kinase signal released from differentiation-dependent control provides a negative stimulus for the onset of myogenic differentiation.

10.1083/jcb.137.5.1057

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Citations (176)

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

Journal of Virology (1989)

Rossella Maione Armando Felsani Laura Pozzi Maurizia Caruso Paolo Amati

The mRNAs for myogenic functions are coordinately transcribed with polyomavirus (Py) early mRNA during in vitro differentiation of mouse C2 myoblast cells. Sequence analysis shows that the A domain of the Py enhancer includes an E1A-like consensus sequence that is also found in the 5' upstream region of two genes expressed during myoblast differentiation: alpha-actin and myosin light chain. Therefore, the coordinate expression of such genes with Py early mRNA may be activated by a common cellular regulatory factor. In the present work, we report that C2 cells surviving Py infection are unable to differentiate and do not express alpha-actin and myosin light-chain mRNAs. Hybrids between such Py-resistant myoblast cells and the parental cells exhibited dominance of the permissibility to Py growth and of the expression of myogenic mRNAs. In C2 cells transiently transfected with a chimeric plasmid (pSVPy12CAT) harboring the bacterial chloramphenicol acetyltransferase (CAT) gene driven by the Py enhancer-promoter region, the CAT gene was expressed irrespective of their stage of differentiation. Moreover, undifferentiated stably transfected cells expressing the CAT gene restricted viral growth. Py-resistant C2 myoblasts transiently transfected with pSVPy12CAT also expressed the CAT gene driven by the Py enhancer. This contradictory finding is similar to results previously obtained by other investigators with cloned genes specific for myogenic functions, and it may be explained by a structural difference between the pSVPy12CAT and the Py genomic organizations in which the viral enhancer operates.

Chloramphenicol acetyltransferase

Enhancer RNAs

Enhancer trap

10.1128/jvi.63.11.4890-4897.1989

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Citations (10)

Inhibition of in vitro muscle differentiation by the immortalizing oncogene py LT-ag.

PubMed (1992)

Rossella Maione Gian María Fimia Paolo Amati

The interference of Polyomavirus (Py) early functions with in vitro myogenic differentiation is the object of this study. Single cell analysis of C2 myogenic Py infected cells showed a mutual exclusion between Py early functions and muscle gene expression. The morphological and biochemical analysis of clones obtained from C2 cells stably transfected with a plasmid carrying an ORI- Py genome, showed that myogenesis is blocked and cells display the transformed phenotype. By using plasmids separately encoding Middle T or Large T functions, the involvement of individual early viral gene products was determined. Py Middle T alone does not inhibit myotube formation even though cells are morphologically transformed. Myogenic differentiation, on the other hand, is inhibited by Py Large T. This inhibition, which is proportional to the level of Py Large T expression, does not entail to require alteration of cell growth properties and acts by blocking the expression of myogenin and terminal differentiation markers without altering the expression of the regulatory gene MyoD.

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Functional interplay between MyoD and CTCF in regulating long-range chromatin interactions during differentiation

Journal of Cell Science (2014)

Cecilia Battistelli Anna Busanello Rossella Maione

Higher-order chromatin structures appear to be dynamically arranged during development and differentiation. However, the molecular mechanism underlying their maintenance or disruption and their functional relevance in gene regulation are poorly understood. We recently described a dynamic long-range chromatin interaction between the gene-promoter of the cdk inhibitor p57kip2 and the imprinting control region KvDMR1 in muscle cells. Here we show that CTCF, the best characterized organizer of long-range chromatin interactions, binds to both p57kip2 promoter and KvDMR1 and is necessary for the maintenance of their physical contact. Moreover, we show that CTCF-mediated looping is required for preventing p57kip2 expression before differentiation. Finally, we provide evidence that the induction of p57kip2 during myogenesis involves the physical interaction of the muscle regulatory-factor MyoD with CTCF at KvDMR1, the displacement of the cohesin complex subunit Rad21 and the destabilization of the chromatin loop. The finding that MyoD affects chromatin looping at CTCF-binding sites represents the first evidence that a differentiation factor regulates chromatin loop dynamics and provides a useful paradigm for gaining insights into the developmental regulation of long-range chromatin contacts.

CTCF

ChIA-PET

Bivalent chromatin

10.1242/jcs.149427

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Citations (33)

MyoD regulates p57 kip2 expression by interacting with a distant cis -element and modifying a higher order chromatin structure

Nucleic Acids Research (2012)

Anna Busanello Cecilia Battistelli Mariarosaria Carbone Cassandra Mostocotto Rossella Maione

The bHLH transcription factor MyoD, the prototypical master regulator of differentiation, directs a complex program of gene expression during skeletal myogenesis. The up-regulation of the cdk inhibitor p57 kip2 plays a critical role in coordinating differentiation and growth arrest during muscle development, as well as in other tissues. p57 kip2 displays a highly specific expression pattern and is subject to a complex epigenetic control driving the imprinting of the paternal allele. However, the regulatory mechanisms governing its expression during development are still poorly understood. We have identified an unexpected mechanism by which MyoD regulates p57 kip2 transcription in differentiating muscle cells. We show that the induction of p57 kip2 requires MyoD binding to a long-distance element located within the imprinting control region KvDMR1 and the consequent release of a chromatin loop involving p57 kip2 promoter. We also show that differentiation-dependent regulation of p57 kip2 , while involving a region implicated in the imprinting process, is distinct and hierarchically subordinated to the imprinting control. These findings highlight a novel mechanism, involving the modification of higher order chromatin structures, by which MyoD regulates gene expression. Our results also suggest that chromatin folding mediated by KvDMR1 could account for the highly restricted expression of p57 kip2 during development and, possibly, for its aberrant silencing in some pathologies.

10.1093/nar/gks619

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Citations (33)

Selection of mouse neuroblastoma cell-specific polyoma virus mutants with stage differentiative advantages of replication.

The EMBO Journal (1985)

Rossella Maione Claudio Passananti Vincenzo De Simone P Delli-Bovi G. Augusti‐Tocco

Replication

Polyoma virus

10.1002/j.1460-2075.1985.tb04068.x

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Citations (31)

Synthesis of a new zinc finger peptide; comparison of its `code' deduced and `CASTing' derived binding sites

FEBS Letters (1997)

Nicoletta Corbi Marie Perez Rossella Maione Claudio Passananti

Using two synthetic oligonucleotides, we have constructed a new gene containing three zinc finger motifs of the Cys 2 ‐His 2 type. We named this artificial gene `Mago'. The Mago nucleotide triplets encoding the amino acid positions, described to be crucial for DNA binding specificity, have been chosen on the basis of the proposed recognition `code' that relates the zinc finger's primary structure to the DNA binding target. Here we demonstrate that Mago protein specifically binds the `code' DNA target, with a dissociation constant ( K d ) comparable to the K d of the well known Zif268 protein with its binding site. Moreover, we show that the deduced Mago `code' and the `experimental' selected DNA binding sites are almost identical, differing only in two nucleotides at the side positions.

Zinc finger nuclease

Protein–DNA interaction

RING finger domain

Genetic Code

10.1016/s0014-5793(97)01257-x

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Citations (25)