Abstract:
:Rett syndrome (RTT) is a neurodevelopmental disorder caused by mutations in the gene encoding MeCP2. By binding to methylated CpG dinucleotide promoter regions, MeCP2 acts as a transcriptional repressor, predicting that its absence might result in widespread aberrant gene transcription, leading to the RTT phenotype. Considering this potentially broad action of MeCP2 on expression and the complexity of the brain, especially during development, we approached the consequences of MeCP2 deficiency in a mouse model by using a temporal and regional proteomic strategy. We used the olfactory system (olfactory epithelium and bulb) because its attributes make it an excellent developmental model system. We find evidence of temporal and regional proteomic pattern differences between WT and MeCP2-deficient mice. It was possible to segregate these changes in protein expression into five biological function groups: cytoskeleton arrangement, chromatin modeling, energy metabolism, cell signaling, and neuroprotection. By combining the proteomic results with the RNA levels of the identified proteins, we show that protein expression changes are the consequence of differences in mRNA level or posttranslational modifications. We conclude that brain regions and ages must be carefully considered when investigating MeCP2 deficiency, and that not only transcription should be taken into account as a source for these changes, but posttranslational protein modifications as well.
journal_name
Proc Natl Acad Sci U S Aauthors
Matarazzo V,Ronnett GVdoi
10.1073/pnas.0307083101keywords:
subject
Has Abstractpub_date
2004-05-18 00:00:00pages
7763-8issue
20eissn
0027-8424issn
1091-6490pii
0307083101journal_volume
101pub_type
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