Primary structure, neural-specific expression, and dendritic location of human BC200 RNA

Tiedge, Henri; Chen, Wei; Brosius, Jürgen

doi:10.1523/jneurosci.13-06-02382.1993

Cited by 218 publications

(230 citation statements)

References 39 publications

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“…How a new RNA gene originated has been explored with interesting insights. Brosius and coworkers have identified two young RNA genes, BC1 and BC200 (5,40), which were created by retroposition tens of millions of years ago (6,7). These genes used adjacent genomic regions as raw materials for new regulatory sequences during the exaptation process for new functions.…”

Section: Discussionmentioning

confidence: 99%

Origin ofsphinx, a young chimeric RNA gene inDrosophilamelanogaster

Wang

Brunet

Nevo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

134

109

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Non-protein-coding RNA genes play an important role in various biological processes. How new RNA genes originated and whether this process is controlled by similar evolutionary mechanisms for the origin of protein-coding genes remains unclear. A young chimeric RNA gene that we term sphinx (spx) provides the first insight into the early stage of evolution of RNA genes. spx originated as an insertion of a retroposed sequence of the ATP synthase chain F gene at the cytological region 60DB since the divergence of Drosophila melanogaster from its sibling species 2-3 million years ago. This retrosequence, which is located at 102F on the fourth chromosome, recruited a nearby exon and intron, thereby evolving a chimeric gene structure. This molecular process suggests that the mechanism of exon shuffling, which can generate protein-coding genes, also plays a role in the origin of RNA genes. The subsequent evolutionary process of spx has been associated with a high nucleotide substitution rate, possibly driven by a continuous positive Darwinian selection for a novel function, as is shown in its sex-and development-specific alternative splicing. To test whether spx has adapted to different environments, we investigated its population genetic structure in the unique ''Evolution Canyon'' in Israel, revealing a similar haplotype structure in spx, and thus similar evolutionary forces operating on spx between environments.

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Section: Discussionmentioning

confidence: 99%

Origin ofsphinx, a young chimeric RNA gene inDrosophilamelanogaster

Wang

Brunet

Nevo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

134

109

View full text Add to dashboard Cite

show abstract

“…In neocortical areas of normal, non-AD brains, BC200 RNA is known to be distributed in a characteristically diffuse manner, resulting from its localization to dendritic domains in neuropil ( Fig. 5B) (2). In contrast, in area 9 of terminal AD brains, the BC200 signal often appeared in conspicuous high-intensity clusters.…”

Section: Somatodendritic Distribution Of Bc200 Rna Is Altered In Sevementioning

confidence: 99%

“…BC RNAs are selectively expressed in neurons and are delivered to synaptodendritic compartments (1,2,(7)(8)(9), where they are thought to contribute to the regulation of local protein synthesis (3,4,6).…”

mentioning

confidence: 99%

Dendritic BC200 RNA in aging and in Alzheimer's disease

Mus¹,

Hof

Tiedge

2007

Proc. Natl. Acad. Sci. U.S.A.

280

199

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Small untranslated BC1 and BC200 RNAs are translational regulators that are selectively targeted to somatodendritic domains of neurons. They are thought to operate as modulators of local protein synthesis in postsynaptic dendritic microdomains, in a capacity in which they would contribute to the maintenance of long-term synaptic plasticity. Because plasticity failure has been proposed to be a starting point for the neurodegenerative changes that are seen in Alzheimer's disease (AD), we asked whether somatodendritic levels of human BC200 RNA are deregulated in AD brains. We found that in normal aging, BC200 levels in cortical areas were reduced by >60% between the ages of 49 and 86. In contrast, BC200 RNA was significantly up-regulated in AD brains, in comparison with age-matched normal brains. This up-regulation in AD was specific to brain areas that are involved in the disease. Relative BC200 levels in those areas increased in parallel with the progression of AD, as reflected by Clinical Dementia Rating scores. In more advanced stages of the disease, BC200 RNA often assumed a clustered perikaryal localization, indicating that dendritic loss is accompanied by somatic overexpression. Mislocalization and overexpression of BC200 RNA may be reactive-compensatory to, or causative of, synaptodendritic deterioration in AD neurons.dementia ͉ non-protein-coding RNA ͉ RNA transport

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“…Following their expression, BC200 RNAs immediately migrate to dendrites, where they interact and interfere with various translational initiation factors, including eIF4A, eIF4B, and PABP. [1][2][3][4][5][6][7] BC200 RNA is thought to exert local translational control by forming distinctive microdomains in dendrites, and this is believed to contribute to the maintenance of neuronal plasticity. BC1 RNA is the rodent counterpart of BC200 RNA 3 ; the 2 together comprise the BC RNAs.…”

Section: Introductionmentioning

confidence: 99%

“…BC200 RNA originated by retro-transposition of an Alu domain, whereas BC1 RNA arose by retroposition of tRNA Ala . 3,8 Although BC200 RNA is normally specific to neuronal dendrites 3 it is abnormally overexpressed under some disease conditions. In Alzheimer disease, for example, BC200 RNA levels are upregulated in specific brain areas associated with the disease, and they increase with disease progression.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of BC200 RNA expression reduces cell migration and invasion by destabilizing mRNA for calcium-binding protein S100A11

et al. 2017

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Although BC200 RNA is best known as a neuron-specific non-coding RNA, it is overexpressed in various cancer cells. BC200 RNA was recently shown to contribute to metastasis in several cancer cell lines, but the underlying mechanism was not understood in detail. To examine this mechanism, we knocked down BC200 RNA in cancer cells, which overexpress the RNA, and examined cell motility, profiling of ribosome footprints, and the correlation between cell motility changes and genes exhibiting altered ribosome profiles. We found that BC200 RNA knockdown reduced cell migration and invasion, suggesting that BC200 RNA promotes cell motility. Our ribosome profiling analysis identified 29 genes whose ribosomal occupations were altered more than 2-fold by BC200 RNA knockdown. Many (> 30%) of them were directly or indirectly related to cancer progression. Among them, we focused on S100A11 (which showed a reduced ribosome footprint) because its expression was previously shown to increase cellular motility. S100A11 was decreased at both the mRNA and protein levels following knockdown of BC200 RNA. An actinomycin-chase experiment showed that BC200 RNA knockdown significantly decreased the stability of the S100A11 mRNA without changing its transcription rate, suggesting that the downregulation of S100A11 was mainly caused by destabilization of its mRNA. Finally, we showed that the BC200 RNAknockdown-induced decrease in cell motility was mainly mediated by S100A11. Together, our results show that BC200 RNA promotes cell motility by stabilizing S100A11 transcripts.

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Primary structure, neural-specific expression, and dendritic location of human BC200 RNA

Cited by 218 publications

References 39 publications

Origin ofsphinx, a young chimeric RNA gene inDrosophilamelanogaster

Origin ofsphinx, a young chimeric RNA gene inDrosophilamelanogaster

Dendritic BC200 RNA in aging and in Alzheimer's disease

Knockdown of BC200 RNA expression reduces cell migration and invasion by destabilizing mRNA for calcium-binding protein S100A11

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