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The Zinc Finger Transcription Factor Sp9 Is Required for the Development of Striatopallidal Projection Neurons

ABSTRACT: Purpose: To assess changes in gene expression profiles from the P0 littermate Sp9Flox/Flox control striatum (including SVZ) and conditional mutant striatum of Drd2-Cre; Sp9Flox/Flox mice. Methods: total RNA was isolated and sequenced from the striatum of the P0 littermate Sp9Flox/Flox control or conditional mutant striatum of Drd2-Cre; Sp9Flox/Flox mice in triplicate using an Illumina high-seq 2500. Raw data was analyzed using TopHat. Genes were considered changed which demonstrated fold-change>=2, and p value <=0.05. Changed genes were then filtered to reveal Sp9 downstream targets which were altered in vivo due to the loss of Sp9 expression. Results: 179 genes were significantly increased and 147 genes were significantly decreased in expression level due to the loss of Sp9 expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE83373 | GEO | 2016/06/16

SECONDARY ACCESSION(S): PRJNA325728

REPOSITORIES: GEO

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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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The Zinc Finger Transcription Factor Sp9 Is Required for the Development of Striatopallidal Projection Neurons

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