http://www.cnr.it/ontology/cnr/individuo/prodotto/ID66237
Spatio-temporal dynamics and localization of MeCP2 and pathological mutants in living cells. (Articolo in rivista)
- Type
- Label
- Spatio-temporal dynamics and localization of MeCP2 and pathological mutants in living cells. (Articolo in rivista) (literal)
- Anno
- 2007-01-01T00:00:00+01:00 (literal)
- Alternative label
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- Marchi M; Guarda A; Bergo A; Landsberger N; Kilstrup-Nielsen C; Ratto GM; Costa M. (literal)
- Pagina inizio
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Note
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- Mario Costa: Istituto di Neuroscienze Pisa
GM Ratto: Istituto Nanoscienze (literal)
- Titolo
- Spatio-temporal dynamics and localization of MeCP2 and pathological mutants in living cells. (literal)
- Abstract
- MECP2 is an X-linked gene? co????? coding fforo?? ??a protp?ote????in fufun?ctcti?on??????????ing as a trt????anscrc??iptpti?on????al
repressor. The protein MeCP2 (Methyl CpG-binding protein) is an abundant component
of pericentric heterochromatin and its mutations or duplications are present in around
80% of patients with a neurological disorder known as Rett Syndrome. Although MeCP2
action depends critically on its binding to chromatin, very little is known about the
dynamics of this process. Using fluorescence recovery after photobleaching in controlled
conditions of protein concentration, we demonstrated that most of the GFP-MeCP2 fusion
protein associates strongly and reversibly to pericentric heterocromatin whereas the
remaining fraction is bound irreversibly. The mobility of the methyl-binding protein is
influenced by the differentiation state of the host cells. Furthermore, residues downstream
of the methyl-binding domain are critical for the interaction with chromatin. Whereas the
binding is stabilised by the central region it is likely modulated by the most C-terminal
region. Importantly, these residues are missing in several disease causing mutations.
Our data suggest that alterations in the affinity of MeCP2 for chromatin might contribute
to the pathological effects of mutations causing Rett Syndrome. (literal)
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