Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from 9 and 13 weeks old TIFIAD1Cre mice

ABSTRACT: We have investigated the p53-dependent stress response in medium spiny neurons (MSNs) that degenerate in Huntington’s disease. To induce p53 signaling cascade, we have genetically inactivated by the Cre/loxP system the essential RNA polymerase I (Pol I) transcription factor TIF-IA, leading to stabilization of p53 and induction of p53-dependent apoptosis. In the present study, we selectively ablated the TIF-IA gene in MSNs by crossing TIF-IAflox/flox mice, homozygous for the floxed TIF-IA allele with transgenic mice expressing the Cre recombinase under the control of the D1 dopamine receptor (D1R) promoter. To explore the molecular mechanisms underlying survival and death we profiled global gene expression in 9 and 13 week old control and TIF-IAD1RCre mutant mice (3 mice/each timepoint For each of the four conditions, five GeneChips were used each )

ORGANISM(S): Mus musculus

SUBMITTER: Grzegorz Kreiner

PROVIDER: E-GEOD-29647 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The striatum is the main input structure of the basal ganglia, receiving information from the cortex and the thalamus and consisting of D1- and D2- medium spiny neurons (MSNs). D1-MSNs and D2-MSNs are essential for motor control and cognitive behaviors and have implications in Parkinson’s Disease. In the present study, we demonstrated that Sp9 positive progenitors produced both D1-MSNs and D2-MSNs and that Sp9 expression was rapidly downregulated in postmitotic D1-MSNs. Furthermore, we found that sustained Sp9 expression in lateral ganglionic eminence (LGE) progenitor cells and their descendants led to promoting D2-MSNs identity and repressing D1-MSNs identity during striatal development. As a result, sustained Sp9 expression resulted in an imbalance between D1-MSNs and D2-MSNs in the mouse striatum. In addition, the fate-changed D2 like-MSNs survived normally in adulthood. Taken together, our finding supported that Sp9 was sufficient to promote D2-MSNs identity and repress D1-MSNs identity, and Sp9 was a negative regulator of D1-MSNs fate. The striatum is the main input structure of the basal ganglia, receiving information from the cortex and the thalamus and consisting of D1- and D2- medium spiny neurons (MSNs). D1-MSNs and D2-MSNs are essential for motor control and cognitive behaviors and have implications in Parkinson’s Disease. In the present study, we demonstrated that Sp9 positive progenitors produced both D1-MSNs and D2-MSNs and that Sp9 expression was rapidly downregulated in postmitotic D1-MSNs. Furthermore, we found that sustained Sp9 expression in lateral ganglionic eminence (LGE) progenitor cells and their descendants led to promoting D2-MSNs identity and repressing D1-MSNs identity during striatal development. As a result, sustained Sp9 expression resulted in an imbalance between D1-MSNs and D2-MSNs in the mouse striatum. In addition, the fate-changed D2 like-MSNs survived normally in adulthood. Taken together, our finding supported that Sp9 was sufficient to promote D2-MSNs identity and repress D1-MSNs identity, and Sp9 was a negative regulator of D1-MSNs fate.

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Expression data from 9 and 13 weeks old TIFIAD1Cre mice

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