Developmental expression of methyl-CpG binding protein 2 is dynamically regulated in the rodent brain

Research output: Contribution to journalArticle

Abstract

The gene encoding methyl-CpG binding protein 2 (MeCP2) is mutated in the large majority of girls that have Rett Syndrome (RTT), an X-linked neurodevelopmental disorder. To better understand the developmental role of MeCP2, we studied the ontogeny of MeCP2 expression in rat brain using MeCP2 immunostaining and Western blots. MeCP2 positive neurons were present throughout the brain at all ages examined, although expression varied by region and age. At early postnatal ages, regions having neurons that were generated early and more mature had the strongest MeCP2 expression. Late developing structures including cortex, hippocampus and cerebellum exhibited the most significant changes in MeCP2 expression. Of these regions, the cerebellum showed the most striking cell-specific changes in MeCP2 expression. For example, the early-generated Purkinje cells became MeCP2 positive by P6, while the late-generated granule cells did not express MeCP2 until the fourth postnatal week. The timing of MeCP2 expression in the granule cell layer is coincident with the onset of granule cell synapse formation. Although more subtle, the degree of MeCP2 expression in cortex and hippocampus was most closely correlated with synaptogenesis in both regions. Our finding that MeCP2 expression is correlated with synaptogenesis is consistent with the hypothesis that Rett Syndrome is caused by defects in the formation or maintenance of synapses.

Original languageEnglish (US)
Pages (from-to)939-949
Number of pages11
JournalNeuroscience
Volume123
Issue number4
DOIs
StatePublished - 2004

Fingerprint

Methyl-CpG-Binding Protein 2
Rodentia
Brain
Rett Syndrome
Synapses
Cerebellum
Hippocampus
Neurons
Purkinje Cells

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Developmental expression of methyl-CpG binding protein 2 is dynamically regulated in the rodent brain. / Mullaney, B. C.; Johnston, Michael V; Blue, Mary E.

In: Neuroscience, Vol. 123, No. 4, 2004, p. 939-949.

Research output: Contribution to journalArticle

@article{8df03bd3a0fa496ebbe96ac26d87c862,
title = "Developmental expression of methyl-CpG binding protein 2 is dynamically regulated in the rodent brain",
abstract = "The gene encoding methyl-CpG binding protein 2 (MeCP2) is mutated in the large majority of girls that have Rett Syndrome (RTT), an X-linked neurodevelopmental disorder. To better understand the developmental role of MeCP2, we studied the ontogeny of MeCP2 expression in rat brain using MeCP2 immunostaining and Western blots. MeCP2 positive neurons were present throughout the brain at all ages examined, although expression varied by region and age. At early postnatal ages, regions having neurons that were generated early and more mature had the strongest MeCP2 expression. Late developing structures including cortex, hippocampus and cerebellum exhibited the most significant changes in MeCP2 expression. Of these regions, the cerebellum showed the most striking cell-specific changes in MeCP2 expression. For example, the early-generated Purkinje cells became MeCP2 positive by P6, while the late-generated granule cells did not express MeCP2 until the fourth postnatal week. The timing of MeCP2 expression in the granule cell layer is coincident with the onset of granule cell synapse formation. Although more subtle, the degree of MeCP2 expression in cortex and hippocampus was most closely correlated with synaptogenesis in both regions. Our finding that MeCP2 expression is correlated with synaptogenesis is consistent with the hypothesis that Rett Syndrome is caused by defects in the formation or maintenance of synapses.",
author = "Mullaney, {B. C.} and Johnston, {Michael V} and Blue, {Mary E}",
year = "2004",
doi = "10.1016/j.neuroscience.2003.11.025",
language = "English (US)",
volume = "123",
pages = "939--949",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "4",

}

TY - JOUR

T1 - Developmental expression of methyl-CpG binding protein 2 is dynamically regulated in the rodent brain

AU - Mullaney, B. C.

AU - Johnston, Michael V

AU - Blue, Mary E

PY - 2004

Y1 - 2004

N2 - The gene encoding methyl-CpG binding protein 2 (MeCP2) is mutated in the large majority of girls that have Rett Syndrome (RTT), an X-linked neurodevelopmental disorder. To better understand the developmental role of MeCP2, we studied the ontogeny of MeCP2 expression in rat brain using MeCP2 immunostaining and Western blots. MeCP2 positive neurons were present throughout the brain at all ages examined, although expression varied by region and age. At early postnatal ages, regions having neurons that were generated early and more mature had the strongest MeCP2 expression. Late developing structures including cortex, hippocampus and cerebellum exhibited the most significant changes in MeCP2 expression. Of these regions, the cerebellum showed the most striking cell-specific changes in MeCP2 expression. For example, the early-generated Purkinje cells became MeCP2 positive by P6, while the late-generated granule cells did not express MeCP2 until the fourth postnatal week. The timing of MeCP2 expression in the granule cell layer is coincident with the onset of granule cell synapse formation. Although more subtle, the degree of MeCP2 expression in cortex and hippocampus was most closely correlated with synaptogenesis in both regions. Our finding that MeCP2 expression is correlated with synaptogenesis is consistent with the hypothesis that Rett Syndrome is caused by defects in the formation or maintenance of synapses.

AB - The gene encoding methyl-CpG binding protein 2 (MeCP2) is mutated in the large majority of girls that have Rett Syndrome (RTT), an X-linked neurodevelopmental disorder. To better understand the developmental role of MeCP2, we studied the ontogeny of MeCP2 expression in rat brain using MeCP2 immunostaining and Western blots. MeCP2 positive neurons were present throughout the brain at all ages examined, although expression varied by region and age. At early postnatal ages, regions having neurons that were generated early and more mature had the strongest MeCP2 expression. Late developing structures including cortex, hippocampus and cerebellum exhibited the most significant changes in MeCP2 expression. Of these regions, the cerebellum showed the most striking cell-specific changes in MeCP2 expression. For example, the early-generated Purkinje cells became MeCP2 positive by P6, while the late-generated granule cells did not express MeCP2 until the fourth postnatal week. The timing of MeCP2 expression in the granule cell layer is coincident with the onset of granule cell synapse formation. Although more subtle, the degree of MeCP2 expression in cortex and hippocampus was most closely correlated with synaptogenesis in both regions. Our finding that MeCP2 expression is correlated with synaptogenesis is consistent with the hypothesis that Rett Syndrome is caused by defects in the formation or maintenance of synapses.

UR - http://www.scopus.com/inward/record.url?scp=1642441427&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1642441427&partnerID=8YFLogxK

U2 - 10.1016/j.neuroscience.2003.11.025

DO - 10.1016/j.neuroscience.2003.11.025

M3 - Article

C2 - 14751287

AN - SCOPUS:1642441427

VL - 123

SP - 939

EP - 949

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

IS - 4

ER -