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Gene expression divergence recapitulates the developmental hourglass model (2010)

A. T. Kalinka ; K. M. Varga ; D. T. Gerrard ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 468(7325): 811-4. doi: 10.1038/nature09634.

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Publication Date: 2010-12-15

Description: The observation that animal morphology tends to be conserved during the embryonic phylotypic period (a period of maximal similarity between the species within each animal phylum) led to the proposition that embryogenesis diverges more extensively early and late than in the middle, known as the hourglass model. This pattern of conservation is thought to reflect a major constraint on the evolution of animal body plans. Despite a wealth of morphological data confirming that there is often remarkable divergence in the early and late embryos of species from the same phylum, it is not yet known to what extent gene expression evolution, which has a central role in the elaboration of different animal forms, underpins the morphological hourglass pattern. Here we address this question using species-specific microarrays designed from six sequenced Drosophila species separated by up to 40 million years. We quantify divergence at different times during embryogenesis, and show that expression is maximally conserved during the arthropod phylotypic period. By fitting different evolutionary models to each gene, we show that at each time point more than 80% of genes fit best to models incorporating stabilizing selection, and that for genes whose evolutionarily optimal expression level is the same across all species, selective constraint is maximized during the phylotypic period. The genes that conform most to the hourglass pattern are involved in key developmental processes. These results indicate that natural selection acts to conserve patterns of gene expression during mid-embryogenesis, and provide a genome-wide insight into the molecular basis of the hourglass pattern of developmental evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kalinka, Alex T -- Varga, Karolina M -- Gerrard, Dave T -- Preibisch, Stephan -- Corcoran, David L -- Jarrells, Julia -- Ohler, Uwe -- Bergman, Casey M -- Tomancak, Pavel -- England -- Nature. 2010 Dec 9;468(7325):811-4. doi: 10.1038/nature09634.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstr. 108, 01307 Dresden, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21150996" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Conserved Sequence/genetics ; Drosophila/classification/*embryology/*genetics ; Drosophila Proteins/genetics ; Evolution, Molecular ; Gene Expression Regulation, Developmental/*genetics ; Genes, Insect/genetics ; Genome, Insect/genetics ; *Models, Biological ; Oligonucleotide Array Sequence Analysis ; Phylogeny ; Selection, Genetic ; Species Specificity ; Time Factors

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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FMRP targets distinct mRNA sequence elements to regulate protein expression (2012)

M. Ascano, Jr. ; N. Mukherjee ; P. Bandaru ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 492(7429): 382-6. doi: 10.1038/nature11737.

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Publication Date: 2012-12-14

Description: Fragile X syndrome (FXS) is a multi-organ disease that leads to mental retardation, macro-orchidism in males and premature ovarian insufficiency in female carriers. FXS is also a prominent monogenic disease associated with autism spectrum disorders (ASDs). FXS is typically caused by the loss of fragile X mental retardation 1 (FMR1) expression, which codes for the RNA-binding protein FMRP. Here we report the discovery of distinct RNA-recognition elements that correspond to the two independent RNA-binding domains of FMRP, in addition to the binding sites within the messenger RNA targets for wild-type and I304N mutant FMRP isoforms and the FMRP paralogues FXR1P and FXR2P (also known as FXR1 and FXR2). RNA-recognition-element frequency, ratio and distribution determine target mRNA association with FMRP. Among highly enriched targets, we identify many genes involved in ASD and show that FMRP affects their protein levels in human cell culture, mouse ovaries and human brain. Notably, we discovered that these targets are also dysregulated in Fmr1(-/-) mouse ovaries showing signs of premature follicular overdevelopment. These results indicate that FMRP targets share signalling pathways across different cellular contexts. As the importance of signalling pathways in both FXS and ASD is becoming increasingly apparent, our results provide a ranked list of genes as basis for the pursuit of new therapeutic targets for these neurological disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528815/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528815/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ascano, Manuel Jr -- Mukherjee, Neelanjan -- Bandaru, Pradeep -- Miller, Jason B -- Nusbaum, Jeffrey D -- Corcoran, David L -- Langlois, Christine -- Munschauer, Mathias -- Dewell, Scott -- Hafner, Markus -- Williams, Zev -- Ohler, Uwe -- Tuschl, Thomas -- HD068546/HD/NICHD NIH HHS/ -- K08 HD068546/HD/NICHD NIH HHS/ -- R01 GM104962/GM/NIGMS NIH HHS/ -- R01 MH080442/MH/NIMH NIH HHS/ -- UL1RR024143/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Dec 20;492(7429):382-6. doi: 10.1038/nature11737. Epub 2012 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of RNA Molecular Biology, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235829" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Base Sequence ; Binding Sites ; Brain/metabolism ; Child ; Child Development Disorders, Pervasive/genetics/metabolism ; Cross-Linking Reagents ; Female ; Fragile X Mental Retardation Protein/*genetics/*metabolism ; Gene Expression Regulation/*genetics ; HEK293 Cells ; Humans ; Immunoprecipitation ; Mice ; Molecular Sequence Data ; Multigene Family ; Mutation ; Ovary/metabolism/pathology ; Protein Biosynthesis/*genetics ; RNA, Messenger/*genetics/metabolism ; Regulatory Sequences, Ribonucleic Acid/*genetics ; Response Elements/genetics ; Signal Transduction ; Substrate Specificity

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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Deregulation of common genes by c-Myc and its direct target, MT-MC1 (2005)

Rogulski, K. R. ; Cohen, D. E. ; Corcoran, D. L. ; [et al.]

National Academy of Sciences

In: PNAS - Proceedings of the National Academy of Sciences of the United States of America. 2005; 102(52): 18968-18973. Published 2005 Dec 19. doi: 10.1073/pnas.0507902102.

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Publication Date: 2005-12-19

Print ISSN: 0027-8424

Electronic ISSN: 1091-6490

Topics: Biology , Medicine , Natural Sciences in General

Published by National Academy of Sciences

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Exhumation charge: The last gasp of a petroleum source rock and implications for unconventional shale resources (2016)

English, J. M., English, K. L., Corcoran, D. V., Toussaint, F.

American Association of Petroleum Geologists (AAPG)

In: AAPG Bulletin

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Publication Date: 2016-01-27

Description: Petroleum (oil and gas) forms from the bacterial or thermal breakdown of kerogen during progressive burial in sedimentary basins. During times of petroleum generation, kerogens in organic-rich source rocks expel petroleum to form a fluid phase in the pore system, capable of migrating under hydrodynamic and buoyancy forces to ultimately escape to the surface or accumulate within petroleum traps in the subsurface. The relative timing of petroleum charge and trap formation is a vital component in the accumulation of petroleum deposits. Exhumed basins have been historically viewed as higher-risk targets for conventional petroleum exploration because of, inter alia, the switch-off of petroleum generation in the source rock at the commencement of cooling during exhumation. However, even at the switch-off point, the source rock may retain a significant volume of petroleum sorbed in kerogen and within its pore system. Herein we demonstrate that if the source rock is exhumed to shallower depths after peak burial, pore pressure reduction and the associated volumetric expansion of the petroleum—particularly of the gaseous—phase in the pore system will result in the discharge of additional petroleum into the adjacent carrier bed or reservoir formations. Because most onshore sedimentary basins are characterized by major exhumation events at some point in their history, this represents an additional and underappreciated mechanism for a late-stage petroleum charge in exhumed sedimentary basins. The modeling also indicates that both the initial, pre-exhumation, total gas storage capacity and the exhumation gas charge are likely to be volumetrically more significant for gas-bearing source rocks that have been exposed to higher initial pressures and lower thermal gradients. The concepts presented here also have implications for petroleum resources retained within unconventional shale reservoirs because high-graded shale plays may be associated with systems where the magnitude or rate of relative overpressure dissipation has limited exhumation charge from the unconventional to conventional reservoirs within the basin.

Print ISSN: 0149-1423

Electronic ISSN: 0149-1423

Topics: Geosciences

Published by American Association of Petroleum Geologists (AAPG)

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Lesions from patients with sporadic cerebral cavernous malformations harbor somatic mutations in the CCM genes: evidence for a common biochemical pathway for CCM pathogenesis (2014)

Mc; Donald, D. A., Shi, C., Shenkar, R., Gallione, C. J., Akers, A. L., Li, S., De Castro, N., Berg, M. J., Corcoran, D. L., Awad, I. A., Marchuk, D. A.

Oxford University Press

In: Human Molecular Genetics

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Publication Date: 2014-07-19

Description: Cerebral cavernous malformations (CCMs) are vascular lesions affecting the central nervous system. CCM occurs either sporadically or in an inherited, autosomal dominant manner. Constitutional (germline) mutations in any of three genes, KRIT1 , CCM2 and PDCD10 , can cause the inherited form. Analysis of CCM lesions from inherited cases revealed biallelic somatic mutations, indicating that CCM follows a Knudsonian two-hit mutation mechanism. It is still unknown, however, if the sporadic cases of CCM also follow this genetic mechanism. We extracted DNA from 11 surgically excised lesions from sporadic CCM patients, and sequenced the three CCM genes in each specimen using a next-generation sequencing approach. Four sporadic CCM lesion samples (36%) were found to contain novel somatic mutations. Three of the lesions contained a single somatic mutation, and one lesion contained two biallelic somatic mutations. Herein, we also describe evidence of somatic mosaicism in a patient presenting with over 130 CCM lesions localized to one hemisphere of the brain. Finally, in a lesion regrowth sample, we found that the regrown CCM lesion contained the same somatic mutation as the original lesion. Together, these data bolster the idea that all forms of CCM have a genetic underpinning of the two-hit mutation mechanism in the known CCM genes. Recent studies have found aberrant Rho kinase activation in inherited CCM pathogenesis, and we present evidence that this pathway is activated in sporadic CCM patients. These results suggest that all CCM patients, including those with the more common sporadic form, are potentially amenable to the same therapy.

Print ISSN: 0964-6906

Electronic ISSN: 1460-2083

Topics: Biology , Medicine

Published by Oxford University Press

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Quantification of biological aging in young adults [Medical Sciences] (2015)

Belsky, D. W., Caspi, A., Houts, R., Cohen, H. J., Corcoran, D. L., Danese, A., Harrington, H., Israel, S., Levine, M. E., Schaefer, J. D., Sugden, K., Williams, B., Yashin, A. I., Poulton, R., Moffitt, T. E.

National Academy of Sciences

In: PNAS - Proceedings of the National Academy of Sciences

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Publication Date: 2015-07-29

Description: Antiaging therapies show promise in model organism research. Translation to humans is needed to address the challenges of an aging global population. Interventions to slow human aging will need to be applied to still-young individuals. However, most human aging research examines older adults, many with chronic disease. As a result,...

Print ISSN: 0027-8424

Electronic ISSN: 1091-6490

Topics: Biology , Medicine , Natural Sciences in General

Published by National Academy of Sciences

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