Deletion of Prdm8 impairs development of upper‐layer neocortical neurons. (18th August 2015)
- Record Type:
- Journal Article
- Title:
- Deletion of Prdm8 impairs development of upper‐layer neocortical neurons. (18th August 2015)
- Main Title:
- Deletion of Prdm8 impairs development of upper‐layer neocortical neurons
- Authors:
- Inoue, Mayuko
Iwai, Ryota
Yamanishi, Emiko
Yamagata, Kazuyuki
Komabayashi‐Suzuki, Mariko
Honda, Aya
Komai, Tae
Miyachi, Hitoshi
Kitano, Satsuki
Watanabe, Chisato
Teshima, Waka
Mizutani, Ken‐ichi - Abstract:
- <abstract abstract-type="main" id="gtc12274-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Upper‐layer (UL) neocortical neurons are the most prominent distinguishing features of the mammalian neocortex compared with those of the avian dorsal cortex and are vastly expanded in primates. However, little is known about the identities of the genes that control the specification of UL neurons. Here, we found that Prdm8, a member of the PR (PRDI‐BF1 and RIZ homology) domain protein family, was specifically expressed in the postnatal UL neocortex, particular those in late‐born RORß‐positive layer IV neurons. We generated homozygous <italic>Prdm8</italic> knockout (<italic>Prdm8 </italic>KO) mice and found that the deletion of Prdm8 causes growth retardation and a reduced brain weight, although the brain weight‐to‐body weight ratio is unchanged at postnatal day 8 (P8). Immunohistochemistry showed that the relative UL thickness, but not the thickness of the deep layer (DL), was significantly reduced in <italic>Prdm8 </italic>KO mice compared with wild‐type (WT) mice. In addition, we found that a number of late‐born Brn2‐positive UL neurons were significantly decreased in <italic>Prdm8 </italic>KO mice. To identify genes regulated by Prdm8 during neocortical development, we compared expression profiling analysis in <italic>Prdm8 </italic>KO and WT mice, and identified some candidate genes. These results suggest that the proper expression of Prdm8 is required for<abstract abstract-type="main" id="gtc12274-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Upper‐layer (UL) neocortical neurons are the most prominent distinguishing features of the mammalian neocortex compared with those of the avian dorsal cortex and are vastly expanded in primates. However, little is known about the identities of the genes that control the specification of UL neurons. Here, we found that Prdm8, a member of the PR (PRDI‐BF1 and RIZ homology) domain protein family, was specifically expressed in the postnatal UL neocortex, particular those in late‐born RORß‐positive layer IV neurons. We generated homozygous <italic>Prdm8</italic> knockout (<italic>Prdm8 </italic>KO) mice and found that the deletion of Prdm8 causes growth retardation and a reduced brain weight, although the brain weight‐to‐body weight ratio is unchanged at postnatal day 8 (P8). Immunohistochemistry showed that the relative UL thickness, but not the thickness of the deep layer (DL), was significantly reduced in <italic>Prdm8 </italic>KO mice compared with wild‐type (WT) mice. In addition, we found that a number of late‐born Brn2‐positive UL neurons were significantly decreased in <italic>Prdm8 </italic>KO mice. To identify genes regulated by Prdm8 during neocortical development, we compared expression profiling analysis in <italic>Prdm8 </italic>KO and WT mice, and identified some candidate genes. These results suggest that the proper expression of Prdm8 is required for the normal development and construction of UL neurons in the mammalian neocortex.</p> </abstract> … (more)
- Is Part Of:
- Genes to cells. Volume 20:Number 9(2015:Sep.)
- Journal:
- Genes to cells
- Issue:
- Volume 20:Number 9(2015:Sep.)
- Issue Display:
- Volume 20, Issue 9 (2015)
- Year:
- 2015
- Volume:
- 20
- Issue:
- 9
- Issue Sort Value:
- 2015-0020-0009-0000
- Page Start:
- 758
- Page End:
- 770
- Publication Date:
- 2015-08-18
- Subjects:
- Cytogenetics -- Periodicals
Cells -- Mechanical properties -- Periodicals
Molecular genetics -- Periodicals
Genes -- Periodicals
Molecular biology -- Periodicals
Cytology -- Periodicals
Biomechanics -- Periodicals
571.6 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-2443 ↗
http://www.blacksci.co.uk/%7Ecgilib/jnlpage.bin?Journal=GTC&File=GTC&Page=aims ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/gtc.12274 ↗
- Languages:
- English
- ISSNs:
- 1356-9597
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4111.762500
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 4103.xml