Expanding the ‘central dogma’: the regulatory role of nonprotein coding genes and implications for the genetic liability to schizophrenia

Perkins, Diana O.; Jeffries, Clark; Sullivan, Patrick

doi:10.1038/sj.mp.4001577

Cited by 91 publications

(68 citation statements)

References 87 publications

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“…Furthermore, the increasing variety of ncRNAs being identified in the CNS suggests a strong connection between the biogenesis, dynamics of action, and combinational regulatory potential of ncRNAs and the complexity of the CNS [134,135]. Therefore, further advances in studies on the mechanisms and consequences of RNA damage and its surveillance may have a significant impact on the understanding of the pathophysiology of currently unresolved complex diseases including neurodegenerative and psychiatric diseases [134,136,137].…”

Section: Rna Oxidation and Repairmentioning

confidence: 99%

Nucleic acid oxidation in Alzheimer disease

Moreira

Nunomura

Nakamura

et al. 2008

Free Radical Biology and Medicine

188

113

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Increasing evidence suggests that oxidative stress is intimately associated with Alzheimer disease pathophysiology. Nucleic acids (nuclear DNA, mitochondrial DNA, and RNA) are one of the several cellular macromolecules damaged by reactive oxygen species, particularly the hydroxyl radical. Because neurons are irreplaceable and survive as long as the organism does, they need elaborate defense mechanisms to ensure their longevity. In Alzheimer disease, however, an accumulation of nucleic acid oxidation is observed, indicating an increased level of oxidative stress and/or a decreased capacity to repair the nucleic acid damage. In this review, we present data supporting the notion that mitochondrial and metal abnormalities are key sources of oxidative stress in Alzheimer disease. Furthermore, we outline the mechanisms of nucleic acid oxidation and repair. Finally, evidence showing the occurrence of nucleic acid oxidation in Alzheimer disease will be discussed.

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Section: Rna Oxidation and Repairmentioning

confidence: 99%

Nucleic acid oxidation in Alzheimer disease

Moreira

Nunomura

Nakamura

et al. 2008

Free Radical Biology and Medicine

188

113

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“…Changes in chromatin that are restricted to neurons cannot lead to heritable changes. Nevertheless, I want to expand this argument by reference to schizophrenia (Perkins et al, 2005;Sharma, 2005), a devastating psychosis that effects around 1% of the population. Schizophrenia is a neurodevelopmental disorder, at least in the mind of many neurobiologists, and since largescale population studies such as those used in the Dutch and Chinese famines show a robust epigenetic component to inheritance (see reply to third question), then we must accept that there is an epigenetic component to development-in this case, the development of behavior.…”

Section: Relatively Few Epigenetically Regulated Developmental Decisimentioning

confidence: 99%

Epigenetics in development

Kiefer

2007

Developmental Dynamics

242

144

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It has become increasingly evident in recent years that development is under epigenetic control. Epigenetics is the study of heritable changes in gene function that occur independently of alterations to primary DNA sequence. The best-studied epigenetic modifications are DNA methylation, and changes in chromatin structure by histone modifications, and histone exchange. An exciting, new chapter in the field is the finding that long-distance chromosomal interactions also modify gene expression. Epigenetic modifications are key regulators of important developmental events, including X-inactivation, genomic imprinting, patterning by Hox genes and neuronal development. This primer covers these aspects of epigenetics in brief, and features an interview with two epigenetic scientists. Developmental Dynamics 236: 1144 -1156, 2007.

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“…Due to the increase in the number of these studies, researchers have initiated investigations of not only of the localization of antisense transcripts but also of regulation of sense transcripts with their antisense transcripts in order to more fully understand the molecular interaction occurring in individual loci, cells and tissues. Changes in the expression levels of each non-coding RNA have been described for complex diseases such as cancer [1,14,17] and neurological diseases [11].However, little is known about the expression of CT sense and antisense pair transcripts during pre-and postnatal development. Hence, in the present study, we selected the above CT-related organs as tissues for a "transcriptomics" investigation and measured the amount of CT mRNA in the tissues over the course of mouse development.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Expression Profile and Localization of Mouse Calcitonin (CT) Sense/Antisense Transcripts in Pre- and Postnatal Tissue Development

Rezaeian

Nishibori

Hiraiwa

et al. 2009

The Journal of Veterinary Medical Science

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ABSTRACT. Calcitonin (CT) has been shown to have various functions including osteoclast activity and calcium and phosphorus metabolism in mammals. In the present study, we measured the amounts of CT mRNA in the mouse brain, liver, kidney, heart and testis at various development stages, 14 days post-coitum (dpc), 17-dpc, newborn, 1 week and 8 weeks (adult), using real-time PCR. In the brain and kidney, the amount of CT mRNA decreased with development. In the testis, elevated amounts were observed at 17-dpc and 8 weeks. In the liver, the amount increased from the 14 dpc embryo to newborn stage and then decreased. In the heart, elevated amounts were observed at 17-dpc. Additionally, the CT antisense transcript was determined using a modified RT-PCR and nucleotide sequencing in the present study. Organs with high mRNA expressions were examined for localization of transcripts using in situ hybridization. The CT sense and antisense transcripts in the 14 dpc brain were mainly localized in the mesencephalon. In the pre-and postnatal stages, sense and antisense transcripts were shown to exist rather uniformly in the kidney, heart, liver and testis. In the 17-dpc rib and thyroid lobe and the adult ovary, the sense and antisense transcripts were found to be densely localized. KEY WORDS: calcitonin, in situ hybridization, mouse, sense/antisense transcripts.J. Vet. Med. Sci. 71 (5): [561][562][563][564][565][566][567][568] 2009 Calcitonin (CT) is a 32 amino acid peptide hormone that has been shown to participate in osteoclast activity and reabsorption of calcium and phosphorus through target organ comprised of the bone and kidney in mammals. CT is mainly produced in parafollicular cells (C cells) in the thyroid gland and is produced in a wide variety of other tissues [12]. Currently, CT is a therapeutic agent for treatment of bone diseases such as osteoporosis and Paget's disease [10,16]. Expression of CT in tissue from the brain, prostate and uterus has been reported [3][4][5], and this suggests that it has additional functions other than those for osteoclasts and the kidney. As supporting evidence for additional functions, the CT expression levels have been shown to be related with tumorigenicity of prostate cancer [15] and to be increased in the pregnant rat uterus during implantation [4]. Furthermore, treatment with antisense olignucleotide of CT mRNA severely impairs embryo implantation [18].In the past several years, the number of sense and antisense pair transcripts reported has sharply increased [7]. Due to the increase in the number of these studies, researchers have initiated investigations of not only of the localization of antisense transcripts but also of regulation of sense transcripts with their antisense transcripts in order to more fully understand the molecular interaction occurring in individual loci, cells and tissues. Changes in the expression levels of each non-coding RNA have been described for complex diseases such as cancer [1,14,17] and neurological diseases [11].However, little is known about th...

show abstract

Expanding the ‘central dogma’: the regulatory role of nonprotein coding genes and implications for the genetic liability to schizophrenia

Cited by 91 publications

References 87 publications

Nucleic acid oxidation in Alzheimer disease

Nucleic acid oxidation in Alzheimer disease

Epigenetics in development

Expression Profile and Localization of Mouse Calcitonin (CT) Sense/Antisense Transcripts in Pre- and Postnatal Tissue Development

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