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At least 19 recordsLinked to original sources
PubMed2005

Stable chromosomal association of MSL2 defines a dosage-compensated nuclear compartment.

Dosage compensation in Drosophila is controlled by a complex (DCC) of proteins and noncoding RNA that binds specifically to the male X chromosome and leads to fine-tuning of transcription. Here, we employ male SL2 cells to characterize DCC function and dynamics during steady state of dosage compensation. Knocking down the key regulator of dosage compensation, male-specific-lethal 2 (MSL2), leads to loss of propagation of histone H4 lysine 16 acetylation and of the twofold elevation of transcription characteristic of the compensated male X chromosome. Surprisingly, lack of dosage compensation does not impair cell viability. Targeting of MSL2 to a reporter gene suffices to initiate dosage compensation in the cell model. Using photobleaching techniques in living cells, we found the association of MSL2 with the X chromosome to be exceptionally stable, essentially excluding dynamic redistribution of the DCC during interphase. This immobility distinguishes MSL2 from most other chromosomal proteins. Our findings have profound implications for the mechanism underlying dosage compensation and furthermore provide a new, conceptual reference of stability in an otherwise highly dynamic nuclear environment.

Acetylation↗
PubMed1993

Adenine phosphoribosyltransferase genes in two Drosophila species: dosage compensation, a nuclear matrix attachment site, and a novel intron position.

The Aprt locus of Drosophila encodes the structural gene for the purine salvage enzyme adenine phosphoribosyltransferase. Aprt is autosomal and enzyme activity is gene-dose-dependent in Drosophila melanogaster. However, Aprt is X-linked and dosage compensated in Drosophila pseudoobscura, as shown here. The Aprt genes of both Drosophila species contain a DNA sequence associated with nuclear matrix attachment sites and these Aprt sequences specifically bind to nuclear matrix in vitro. Putative promoter sequences positioned upstream of the predicted transcriptional start site in the two Aprt genes have a similar structure of direct repeats with an overlapping dyad symmetry, but the DNA sequence of these motifs is not conserved between the two species. Biological features in mutants of Aprt as well as natural variants suggest that dosage compensation of this gene in Drosophila pseudoobscura is due to a general control mechanism on X-linked genes rather than a gene-specific mechanism.

Adenine Phosphoribosyltransferase↗
PubMed2026

Disruption of mitonuclear coadaptation and compensatory evolution after an extreme dietary shift in carnivorous butterflies.

Mitochondrial function depends on tight coordination between mitochondrial and nuclear genomes, which requires long-term coevolution to maintain mitonuclear coadaptation. While mitonuclear incompatibility is typically studied in the context of hybridization, other evolutionary scenarios that may disrupt coadaptation between the two genomes remain less explored. Here, we propose that extreme ecological niche shifts may disrupt mitonuclear coadaptation, which we test in carnivorous Miletinae butterflies with an extreme dietary transition. By generating high-quality genome assemblies, we found that Miletinae exhibit extensive chromosomal rearrangements. Comparative phylogenomic analyses revealed a striking asymmetric mitonuclear evolutionary response: Miletinae exhibit elevated mitochondrial nucleotide substitution rates compared to phytophagous relatives, whereas nuclear rates remain stable. This shift reverses the typical lepidopteran pattern where nuclear rates exceed mitochondrial rates. Interestingly, this mitochondrial acceleration is driven primarily by relaxed purifying selection rather than positive selection. To sustain mitochondrial function, the nuclear genome of Miletinae underwent pervasive, multilayered compensatory evolution. We detected strong signatures of positive selection and accelerated evolution in nuclear genes directly interacting with mitochondrial components across oxidative phosphorylation (OXPHOS) complexes, the mitochondrial translation, and replication and transcription machinery. Furthermore, this nuclear compensatory response extends to systems governing mitochondrial homeostasis, including protein quality control and RNA degradation and stabilization. Our results support a model in which extreme ecological transitions can disrupt ancestral mitonuclear coadaptation and promote the emergence of a new coadapted state through systemic nuclear compensation. This study broadens the conceptual framework of mitonuclear coevolution and highlights its role in facilitating evolutionary persistence after major ecological shifts.

Animals↗
PubMed1987

Maternally transmitted antigens are codominantly expressed by mouse cells containing two kinds of mitochondrial DNA.

Mtf, a cytoplasmic, probably mitochondrial factor, controls Mta polymorphism. We tested for dominance between two forms of Mtf to determine whether Mta is controlled by positive or negative genetic mechanisms. We fused Mtf-disparate cells containing distinct mtDNA markers and selected for hybrids containing both. Such mtDNA heteroplasmons codominantly and stably express alternative Mta antigens. Stable codominance excludes negative genetic mechanisms as well as a model of induced nuclear compensation, and implies Mtf controls Mta expression through a positive genetic mechanism.

Animals↗
PubMed1998

A review of probability of causation and its use in a compensation scheme for nuclear industry workers in the United Kingdom.

The assumption that any additional exposure to ionizing radiation leads to an increase in the risk of stochastic health effects implies that some cases of these effects will be caused by exposure incurred occupationally. The main health effect expected to arise in the exposed individuals is cancer. Such radiation-induced cancers cannot be distinguished from the far larger number of background cancers, and, therefore, causation must be assessed statistically. The probability of causation methodology has been developed to ascertain the likelihood that a particular cancer may be attributed to a particular prior exposure to radiation. Given the pertinent details of an individual case, a probability of causation value is calculated from the appropriate relative risk obtained from radiation risk models derived from the epidemiological study of exposed populations, although there are many uncertainties inherent in a particular probability of causation calculation. In the United Kingdom, the Compensation Scheme for Radiation-linked Diseases has been created to determine whether those individuals occupationally exposed to radiation in the nuclear industry who have subsequently developed a malignant disease should be compensated. The Scheme is a voluntary arrangement based upon the probability of causation methodology, which incorporates various procedures agreed by employer and employee representatives and their advisers. In a pragmatic approach to compensation, the uncertainties of a specific probability of causation calculation are accommodated through generosity factors which favor the claimant and encourage the use of the Scheme. The Scheme, which was introduced in 1982 and modified in 1987 and 1991 in the light of operational experience and revised risk estimates, has provided a successful alternative to litigation from the point of view of both employer and employee.

Humans↗
PubMed2004

Emergency preparedness and response: compensating victims of a nuclear accident.

The 1986 tragedy at the Chernobyl Nuclear Power Plant in Ukraine motivated the entire international nuclear community to ensure that countries would, in the future, be well prepared to manage the physical, psychological and financial consequences of a serious nuclear accident. Since that event, numerous nuclear emergency preparedness and post-emergency management programmes have been established at national and international levels to ensure that appropriate mechanisms will respond to the threat, and the aftermath, of a nuclear accident. The INEX 2000 Workshop on the Indemnification of Nuclear Damage, jointly organised by the OECD/Nuclear Energy Agency and the French Government, was the first ever international programme to address the manner in which victims of a nuclear accident with trans-boundary consequences would be compensated for damage suffered before, during and after the accident. The Workshop results revealed striking differences in the compensation principles and practices implemented in the 30 participating countries, in the co-ordination measures between different public authorities within an affected state, and in the co-operative procedures between the accident state and its neighbours. All participants agreed on the need for improvement in these areas, particularly for maintaining public confidence in governments' ability to properly manage nuclear emergencies.

Compensation and Redress↗
PubMed2005

Effects of chronic infusion of a GABAA receptor agonist or antagonist into the vestibular nuclear complex on vestibular compensation in the guinea pig.

The aim of this study was to determine the effects of chronic infusion of a GABA(A) receptor agonist/antagonist into the ipsilateral or contralateral vestibular nuclear complex (VNC) on vestibular compensation, the process of behavioral recovery that occurs after unilateral vestibular deafferentation (UVD). This was achieved by a mini-osmotic pump that infused, over 30 h, muscimol or gabazine into the ipsilateral or contralateral VNC. Spontaneous nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT) were measured. Infusion of muscimol or gabazine into either the ipsilateral or the contralateral VNC had little effect on SN compensation. In contrast, infusion of muscimol (250, 500, and 750 ng) into the contralateral VNC and gabazine (31.25, 62.5, and 125 ng) into the ipsilateral VNC significantly affected YHT and RHT (p < 0.05), but not their rate of compensation (p > 0.05). Interestingly, the effects of muscimol and gabazine on YHT and RHT were consistent throughout the first 30 h post-UVD. Infusion of muscimol (62.5, 125, and 250 ng) into the ipsilateral VNC and gabazine (125, 375, and 750 ng) into the contralateral VNC had little effect on YHT and RHT or their rate of compensation. These results suggest that the ipsilateral gabazine and contralateral muscimol infusions are modifying the expression of the symptoms without altering the mechanism of compensation. Furthermore, the neurochemical mechanism responsible for vestibular compensation can cope with the both the GABA(A) receptor-mediated and the UVD-induced decrease in resting activity.

Animals↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMed2002

In vitro production and nuclear transfer affect dosage compensation of the X-linked gene transcripts G6PD, PGK, and Xist in preimplantation bovine embryos.

Equal expression of X-linked genes such as G6PD and PGK in females and males and the initiation of X-chromosome inactivation are critically dependent on the expression of the X-inactive specific transcript (Xist). The objective of the present study was to determine the effects of in vitro production (IVP) and nuclear transfer (NT) on the relative abundance (RA) of the X-linked transcripts G6PD, PGK, and Xist in preimplantation bovine embryos. In experiment 1, sex-determined IVP or in vivo-produced embryos were analyzed for mRNA expression of the 3 genes. The sex ratio was 36% vs. 64% in IVP blastocysts and thus deviated significantly from the expected ratio of 50% in the vivo control group. The RA of G6PD transcripts was significantly higher in female IVP embryos than in male embryos. In contrast, no significant differences were seen between in vivo-derived female embryos and their male counterparts. At the morula stage, female IVP embryos transcribed significantly more PGK mRNA than did male embryos. However, blastocysts did not exhibit significant differences in PGK transcripts. No differences were observed for in vivo-derived embryos with regard to the RA of PGK transcripts. The RA of Xist mRNA was significantly higher in all female embryos than in their male counterparts. In experiment 2, IVP, in vivo-developed, NT-derived, and parthenogenetic embryos carrying two X chromosomes of either maternal and paternal origin or of maternal origin only (parthenogenotes) were analyzed for the RA of the 3 genes. In NT-derived morulae, the RA of G6PD transcripts was significantly increased compared with their IVP and in vivo-generated counterparts. G6PD transcript levels were significantly increased in IVP blastocysts compared with in vivo-generated and parthenogenetic embryos. At the morula stage, PGK transcripts were similar in all groups, but the RA of PGK transcripts was significantly higher in IVP blastocysts than in their in vivo-generated, parthenogenetic, and NT-derived counterparts. The RA of Xist was significantly elevated in NT-derived morulae compared with IVP, in vivo-generated, and parthenogenetic embryos. NT-derived blastocysts showed an increased Xist expression compared with that of IVP, in vivo-generated, and parthenogenetic embryos. Results of the present study show for the first time that differences in X-chromosome-linked gene transcript levels are related to a perturbed dosage compensation in female and male IVP and female NT-derived embryos. This finding warrants further studies to improve IVP systems and NT protocols to ensure the production of embryos with normal gene expression patterns.

Animals↗
PubMed1996

A neural network simulation of the vestibular system: implications on the role of intervestibular nuclear coupling during vestibular compensation.

Previous neural network simulations of the vestibular system have been based loosely on known physiology. This research involved the use of a strongly physiologically based neural network model which was used to investigate the role of the vestibular commissure in restoring the bilateral symmetry of the resting rates of the vestibular nuclei during vestibular compensation following unilateral labyrinthectomy. It was found the readjustments in the gain of the vestibular commissure were not primarily responsible for vestibular compensation, as has previously been suggested, but rather that it was modifications in extralabyrinthine sources of tone which mediated the restoration of the central symmetry between the two nuclei.

Animals↗
PubMed1986

[Nuclear-mitochondrial interactions in yeasts: mitochondrial mutations compensating the respiration deficiency of sup1 and sup2 mutants].

An approach to the study of nuclear-mitochondrial interactions is reported. A number of spontaneous mutations compensating the respiratory deficiency in nuclear ribosomal suppressor mutants sup1 and sup2 were obtained and analysed. Among mutations analysed, mitochondrial as well as nuclear ones were found. Mitochondrial mutations neutralizing the expression of nuclear mutations were identified using the cytoduction test and their meiotic inheritance. The interaction of these mutations with sup1 and sup2 mutations resulting in restoration of respiratory competence was gene and allele nonspecific. Earlier we proposed that the respiratory deficiency of sup1 and sup2 mutants reflects the participation of sup1 and sup2 proteins not only in cytoplasmic, but also in mitochondrial translation. The interactions revealed open up the possibility of experimental examination of this hypothesis by means of identification of mitochondrial genes bearing compensating mutations.

DNA, Fungal↗