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Desmosterol in brain is elevated because DHCR24 needs REST for Robust Expression but REST is poorly expressed.

G S Tint¹, Luxing Pan, Quan Shang

¹Research Service, Department of Veterans Affairs Medical Center, East Orange, N.J., USA.

Developmental Neuroscience

|May 28, 2014

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The RE1-silencing transcription factor (REST) unexpectedly enhances fetal brain cholesterol synthesis by upregulating DHCR24. This mechanism, involving REST binding near SREBP, ensures sufficient desmosterol during neural development.

Area of Science:

Neuroscience
Molecular Biology
Biochemistry

Background:

Fetal brain cholesterol synthesis is crucial for development.
DHCR24 (24-dehydrocholesterol reductase) activity is insufficient in the fetal brain, leading to temporary desmosterol accumulation.
The regulation of DHCR24 in neural tissue is not fully understood.

Purpose of the Study:

To investigate the regulatory mechanism of DHCR24 in fetal brain cholesterol synthesis.
To determine the role of the RE1-silencing transcription factor (REST) in DHCR24 gene expression.
To elucidate how REST influences desmosterol precursor levels during neural development.

Main Methods:

Analysis of DHCR24 and REST mRNA levels in fetal mouse brain and liver.
Chromatin immunoprecipitation assays to assess REST binding to the DHCR24 promoter.

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Reporter assays using human DHCR24 promoter constructs with wild-type and mutated RE1 sequences.

Gene silencing experiments to evaluate the effect of REST on DHCR24 expression and sterol levels in HeLa cells.

Main Results:

REST binds to the human DHCR24 promoter near the RE1 sequence, enhancing DHCR24 transcription.
DHCR24 and REST mRNA levels are significantly lower in fetal mouse brain compared to liver.
Silencing REST reduces DHCR24 mRNA and protein, increasing precursor sterols, while DHCR7 and HMGR remain unaffected.
REST and SREBP binding sites (RE1 and SRE) are contiguous on the DHCR24 promoter.

Conclusions:

REST plays a surprising role in upregulating DHCR24 in the fetal brain, despite its generally reduced levels in neural tissues.
The proximity of REST and SREBP binding sites suggests a cooperative mechanism for amplifying DHCR24 expression.
This REST-mediated regulation of DHCR24 likely ensures adequate desmosterol availability for crucial neural development stages.