Activity-dependent regulation of BRINP family genes

Motomiya, Makoto; Kobayashi, Miwako; Iwasaki, Norimasa; Minami, Akio; Matsuoka, Isao

doi:10.1016/j.bbrc.2006.11.072

Cited by 9 publications

(6 citation statements)

References 24 publications

(26 reference statements)

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“…Overexpression of DBCCR-1 suppresses tumour cell growth. Involved in neuronal development (Motomiya et al, 2007) Also referred to as FAM5 family of proteins. EPCS50 EPCS50 EPCS50 expressed in the trophoblast upon implantation of the murine embryo (Hemberger et al, 2000)…”

Section: Sea Anemone Toxinsmentioning

confidence: 99%

The MACPF/CDC family of pore-forming toxins

Rosado

Kondos

Bull³

et al. 2008

Cellular Microbiology

242

207

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SummaryPore-forming toxins (PFTs) are commonly associated with bacterial pathogenesis. In eukaryotes, however, PFTs operate in the immune system or are deployed for attacking prey (e.g. venoms). This review focuses upon two families of globular protein PFTs: the cholesterol-dependent cytolysins (CDCs) and the membrane attack complex/perforin superfamily (MACPF). CDCs are produced by Gram-positive bacteria and lyse or permeabilize host cells or intracellular organelles during infection. In eukaryotes, MACPF proteins have both lytic and non-lytic roles and function in immunity, invasion and development. The structure and molecular mechanism of several CDCs are relatively well characterized. Pore formation involves oligomerization and assembly of soluble monomers into a ring-shaped pre-pore which undergoes conformational change to insert into membranes, forming a large amphipathic transmembrane b-barrel. In contrast, the structure and mechanism of MACPF proteins has remained obscure. Recent crystallographic studies now reveal that although MACPF and CDCs are extremely divergent at the sequence level, they share a common fold. Together with biochemical studies, these structural data suggest that lytic MACPF proteins use a CDC-like mechanism of membrane disruption, and will help understand the roles these proteins play in immunity and development.

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Section: Sea Anemone Toxinsmentioning

confidence: 99%

The MACPF/CDC family of pore-forming toxins

Rosado

Kondos

Bull³

et al. 2008

Cellular Microbiology

242

207

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“…Since BRINP1-mRNA was highly expressed in the hippocampus and further up-regulated in the dentate gyrus in an activity-dependent manner [4,6], we examined the course of differentiation of dentate granule neurons in BRINP1-KO to elucidate the biological basis of the abnormal behavior.…”

Section: Resultsmentioning

confidence: 99%

“…Among the three family members, BRINP1 is most widely expressed in various mouse brain regions including hippocampus, and its expression in adult hippocampus is further up-regulated by the increase of neural activity [6]. In addition to the promoted neurogenesis in hippocampus, BRINP1-KO mice showed a set of abnormal behaviors comparable to the symptoms of human psychiatric disorders.…”

Section: Discussionmentioning

confidence: 99%

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Absence of BRINP1 in mice causes increase of hippocampal neurogenesis and behavioral alterations relevant to human psychiatric disorders

et al. 2014

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BackgroundWe have previously identified BRINP (BMP/RA-inducible neural-specific protein-1, 2, 3) family genes that possess the ability to suppress cell cycle progression in neural stem cells. Of the three family members, BRINP1 is the most highly expressed in various brain regions, including the hippocampus, in adult mice and its expression in dentate gyrus (DG) is markedly induced by neural activity. In the present study, we generated BRINP1-deficient (KO) mice to clarify the physiological functions of BRINP1 in the nervous system.ResultsNeurogenesis in the subgranular zone of dentate gyrus was increased in BRINP1-KO mice creating a more immature neuronal population in granule cell layer. The number of parvalbumin expressing interneuron in hippocampal CA1 subregion was also increased in BRINP1-KO mice. Furthermore, BRINP1-KO mice showed abnormal behaviors with increase in locomotor activity, reduced anxiety-like behavior, poor social interaction, and slight impairment of working memory, all of which resemble symptoms of human psychiatric disorders such as schizophrenia and attention–deficit/hyperactivity disorder (ADHD).ConclusionsAbsence of BRINP1 causes deregulation of neurogenesis and impairments of neuronal differentiation in adult hippocampal circuitry. Abnormal behaviors comparable to those of human psychiatric disorders such as hyperactivity and poor social behavior were observed in BRINP1-KO mice. These abnormal behaviors could be caused by alteration of hippocampal circuitry as a consequence of the lack of BRINP1.

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“…However, considering that BRINP2 and BRINP3 are already moderately expressed in the ES‐derived NSCs and that BRINP1 is more extensively and intensively expressed throughout the CNS neurons, the induction of BRINP1 at the stage of neuronal differentiation may be more critical for the cessation of cell cycle progression in terminally differentiated neurons. Additionally, BRINP1 is also induced in an activity‐dependent manner in mature dentate gyrus where neurogenesis continues into adulthood (Eriksson et al, 1998; Motomiya et al, 2007). Furthermore, it has been reported that neurogenesis in adult dentate gyrus is accelerated by neural activity (Bruel‐Jungerman et al, 2007; Ge et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Analysis of the expression and function of BRINP family genes during neuronal differentiation in mouse embryonic stem cell‐derived neural stem cells

Terashima

Kobayashi

Motomiya

et al. 2009

J of Neuroscience Research

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We previously identified a novel family of genes, BRINP1, 2, and 3, that are predominantly and widely expressed in both the central nervous system (CNS) and peripheral nervous system (PNS). In the present study, we analyzed the expression pattern of three BRINP genes during differentiation of mouse embryonic stem (ES) cell-derived neural stem cells (NSCs) and their effects on the cell-cycle regulation of NSCs. While there was no significant expression of any BRINP-mRNA expressed in mouse ES cells, BRINP 1 and 2-mRNAs was expressed at high levels in the ES cell-derived neural stem cells. Upon differentiation into neuronal cells in the presence of retinoic acid and BDNF, all three types of BRINP-mRNA were induced with a similar time course peaking at day three of treatment. Upon differentiation into astroglial cells in the presence of serum, BRINP1-mRNA was slightly up-regulated, while BRINP2- and BRINP3-mRNAs were almost abolished in the astrocytes. While 69.2, 26.1, and 7.7% of cells in a population of NSCs in the exponentially growing phase were in the G1, S and G2 phases, respectively, over-expression of any one of the three BRINP genes completely abolished cells in the G2 phase and significantly reduced the cells in S phase to 11.8-13.8%. Based on these results, the physiological roles of induced BRINP genes in the cell-cycle suppression of terminally differentiated post-mitotic neurons are discussed.

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Activity-dependent regulation of BRINP family genes

Cited by 9 publications

References 24 publications

The MACPF/CDC family of pore-forming toxins

The MACPF/CDC family of pore-forming toxins

Absence of BRINP1 in mice causes increase of hippocampal neurogenesis and behavioral alterations relevant to human psychiatric disorders

Analysis of the expression and function of BRINP family genes during neuronal differentiation in mouse embryonic stem cell‐derived neural stem cells

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