DOSAGE compensation is an essential, chromosome-wide regulatory process that equalizes expression of most X-linked genes between males (usually XO or XY) and females (usually XX), despite their two-fold difference in X chromosome dose. Flies, worms, and mammals utilize diverse mechanisms of dosage compensation, but all involve global changes in X chromosome structure that ultimately serve to adjust the level of X-linked transcripts in only one sex (Cline and Meyer 1996; Meller 2000; Meyer 2000). These X chromosome changes are mediated by dosage compensation machinery that must recognize and associate specifically with the X chromosome(s) of only the dosage-compensating sex. Although the identity and properties of proteins and noncoding RNAs that execute dosage compensation are known in detail, much less is known about the cis-acting factors that must reside on the X chromosome to recruit the dosage compensation machinery. Important advances in understanding the problem of X chromosome ...
In the current study, we identified dpy-21 and the dosage compensation complex (DCC) as negative regulators of development acting downstream of the TORC2/SGK-1 pathway. dpy-21 suppressed rict-1 developmental delay in a reverse genetic, RNAi screen of candidate SGK-1 targets. dpy-21 has been broadly characterized in C. elegans as a member of the DCC, which is involved in downregulation of the hermaphroditic X chromosome by 50% in order to prevent overexpression of potentially toxic X-linked genes (Yonker and Meyer, 2003; Meyer, 2005). We find in this study that wild-type dpy-21 operates downstream of the TORC2 pathway to regulate developmental rate in larval stage worms, to increase body fat and to reduce brood size. Thus, reduction in function of dpy-21 or other members of the DCC by RNAi in rict-1 mutants reverses the slow developmental rate, lowers body fat and raises brood size. RNAi to dpy-21, however, has negative effects on rict-1 mutant body size and longevity, resulting in a reduced ...
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p,Chromatin entry sites (CES) are 100- to 1,500-bp elements that recruit male-specific lethal (MSL) complexes to the X chromosome to upregulate expression of X-linked genes in male flies. CES contain one or more ∼20-bp GA-rich sequences called MSL recognition elements (MREs) that are critical for dosage compensation. Recent studies indicate that CES also correspond to boundaries of X-chromosomal topologically associated domains (TADs). Here, we show that an ∼1,000-kDa complex called the late boundary complex (LBC), which is required for the functioning of the Bithorax complex boundary , interacts specifically with a special class of CES that contain multiple MREs. Mutations in the MRE sequences of three of these CES that disrupt function abrogate interactions with the LBC. Moreover, reducing the levels of two LBC components compromises MSL recruitment. Finally, we show that several of the CES that are physically linked to each other are LBC interactors.,/p,. ...
In the fruitfly Drosophila melanogaster, the four male-specific lethal (msl) genes are required to achieve dosage compensation of the male X chromosome. The MSL proteins are thought to interact with cis-acting sites that confer dosage compensation to nearby genes, as they are detected at hundreds of discrete sites along the length of the polytene X chromosome in males but not in females. The histone H4 acetylated isoform, H4Ac16, colocalizes with the MSL proteins at a majority of sites on the D. melanogaster X chromosome. Using polytene chromosome immunostaining of other species from the genus Drosophila, we found that X chromosome association of MSL proteins and H4Ac16 is conserved despite differences in the sex chromosome karyotype between species. Our results support a model in which cis-acting regulatory sites for dosage compensation evolve on a neo-X chromosome arm in response to the degeneration of its former homologue.. ...
Dosage compensation in Drosophila involves the assembly of the MSL-2-containing dosage compensation complex (DCC) on the single X chromosome of male flies. Translational repression of msl-2 mRNA blocks this process in females. The ubiquitous protein Upstream of N-ras (Unr) is a necessary co-factor for msl-2 repression in vitro. In mammals Unr interacts with PABP (see Drosophila Pabp) within complexes that bind to distinct regions in the target transcripts. This study explored the function of Drosophila Unr in vivo. Hypomorphic Unr mutant flies show DCC assembly on high-affinity sites in the female X chromosomes, confirming that Unr inhibits dosage compensation in female flies. Unexpectedly, male mutant flies and Unr-depleted SL2 cells show decreased DCC binding to the X chromosome, suggesting a role for Unr in DCC assembly or targeting. Consistent with this possibility, Unr overexpression results in moderate loss of DCC from the male X chromosome and predominant male lethality. ...
Home » Lympholeukocyte » Lymphoma b-cell » Lymphoma diffuse » Lymphopenia » Lyonization. Lyonization The inactivation of an x chromosome. One of the two x chromosomes in every cell in a female is randomly inactivated early in embryonic development. Named after geneticist mary lyon. ...
Dosage Compensation in Organisms with Heterogametic Males, Sex Determination, Sex Differentiation, Dosage Compensation and Genetic Imprinting, Genetics
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The Drosophila MSL complex mediates dosage compensation by increasing transcription of the single X chromosome in males approximately two-fold. This is accomplished through recognition of the X chromosome and subsequent acetylation of histone H4K16 on X-linked genes. Initial binding to the X is thought to occur at "entry sites" that contain a consensus sequence motif ("MSL recognition element" or MRE). However, this motif is only similar to 2 fold enriched on X, and only a fraction of the motifs on X are initially targeted. Here we ask whether chromatin context could distinguish between utilized and non-utilized copies of the motif, by comparing their relative enrichment for histone modifications and chromosomal proteins mapped in the modENCODE project. Through a comparative analysis of the chromatin features in male S2 cells (which contain MSL complex) and female Kc cells (which lack the complex), we find that the presence of active chromatin modifications, together with an elevated local GC ...
Detail záznamu - Atnoa1 mutant Arabidopsis plants induce compensation mechanisms to reduce the negative effects of the mutation - Detail záznamu - Knihovna Akademie věd České republiky
Usually we are surprised if we unmask the secret double life of a close friend of who we thought we knew well. Researchers of the Max Planck Institute of Immunobiology and Epigenetics in Freiburg have such a special friend. Its name is the "MSL complex" and the scientists were just recently able to reveal a new exciting facet of its "personality".. The MSL complex is a particular set of proteins and non-coding RNAs that is already known for mediating dosage compensation in flies. Dosage compensation is a necessary molecular balancing mechanism to guarantee that males (XY) and females (XX) produce the same amount of proteins from the genes encoded on the X chromosome despite the difference in the number of X chomosomes. The lab of Asifa Akhtar is investigating the role of the MSL complex as major player in dosage compensation in Drosophila melanogaster. Here, the daily life of the MSL complex is to upregulate the activity of gene transcription of the single male X chromosome to balance the ...
We showed that a set of X-linked genes called X-signal elements (XSEs) communicates X-chromosome dose by repressing the master sex-determination switch gene xol-1 in a cumulative, dose-dependent manner. XOL-1, a GHMP kinase, is activated in 1X:2A embryos (1 dose of XSEs) to set the male fate but repressed in 2X:2A embryos (2 doses of XSEs) to promote the hermaphrodite fate, including the activation of X-chromosome dosage compensation. We also showed that the dose of autosomes is communicated by a set of autosomal signal elements (ASEs) that also act in a cumulative, dose-dependent manner to counter XSEs by stimulating xol-1 transcription. We have explored the biochemical basis by which XSEs counter ASEs to determine sex. Analysis in vitro showed that XSEs (nuclear receptors and homeodomain proteins) and ASEs (T-box and zinc-finger proteins) bind directly to at least 5 distinct sites in xol-1 regulatory DNA to counteract each others activities and thereby regulate xol-1 transcription (Figure 2). ...
All organisms must regulate their genes precisely for normal development and to prevent disease states. However, significant gene copy number variation exists a...
X-linked gene expression in somatic cell hybrids before and after expression of XIST/Xist.(A-C) Shows the XIST/Xist expression in cell nuclei using RNA FISH p
Single embryo RNA-seq combined with mouse genetics provides a comprehensive view on the roles of Rlim and Xist for the regulation of X-linked gene expression during early mouse embryogenesis.
A color cathode-ray tube apparatus has a compensation mechanism for generating a magnetic field that compensates a change in a horizontal-deflection magnetic field due to a change in the temperature of horizontal-deflection coils. The compensation mechanism is formed of auxiliary coils to which a current is supplied in synchronism with horizontal deflection of electron beams, and a control element for controlling the current supplied to the auxiliary coils in accordance with a change in the temperature of the horizontal-deflection coils.
Video created by The University of Melbourne for the course Epigenetic Control of Gene Expression. X chromosome inactivation is a really well-characterised epigenetic process that is now used as a model system to study epigenetic processes that ...
Sex determination in Drosophila is based on the ratio of sex chromosomes to autosomes. If the ratio equals 1, i.e. 2X chromosomes are present, the fly is female via the activation of Sxl gene. Whereas, if the ratio is 0.5, i.e. a single X chromosome is present, the fly is male and Sxl gene is not activated. Therefore, Sxl is a significant factor in determining the sex of Drosophila. The Sxl protein binds to the pre-mRNA of transformer and affects its splicing2. Overall, leading to female-specific physical characteristics and prevention of dosage compensation1. The modification, m6A is caused by the methylosome which is a protein complex that methylates adenosines within the mRNA. The methylosome in flies contains METTL14, Ime4 (Inducer of meiosis 4), KAR4 (Karyogamy protein 4), Female-lethal (2)d (Fl(2)d) and Virilizer (Vir)3.The biological effects of this alteration are dependent on protein readers such as YT521-B; which binds to m6A and mediate its effects on alternative splicing4. The ...
Video created by 墨尔本大学 for the course 基因表达的表观遗传调控. X chromosome inactivation is a really well-characterised epigenetic process that is now used as a model system to study epigenetic processes that are relevant more broadly. This is because it ...
LincRNAs are pervasively transcribed in the genome, although their role in health and disease is poorly understood. Studies of dosage compensation, imprinting and homeotic gene expression suggest that lincRNAs function at the interface between DNA and chromatin remodeling with further involvement in reprogramming of chromatin to promote cancer metastasis. To date a range of different interactions have been hypothesized for lincRNAs in transcriptional regulation, and they may function both as intact interacting molecules as well as Dicer processed molecules that are chopped into small interfering RNAs that degrade other RNAs.. Chromatin remodeling can be analyzed by the marks left by histones on the DNA strand, which can be of either permissive or repressive nature, depending on the acetylation or methylation taking place of the histones. As an example, trimethylation of lysine 4 on histone H3 (H3K4me3) is enriched at transcriptionally active gene promoters, whereas trimethylation of H3K9 ...
The saturation of visual scene decreases by haze due to environments (e.g. fog) and optical properties of eyes (e.g. aging of crystalline lens). However, we would be able to maintain stable colorfulness perception of a scene if we have a mechanism to compensate deceased saturation by haze. We previously examined the influence of haze on the colorfulness perception of natural images using foggy filters, and showed that it was almost the same with and without the foggy filters even immediately after wearing the filters, suggesting a strong instantaneous colorfulness compensation mechanism (ICVS2015). Here, we further examine if the strength of colorfulness compensation is influenced by the pattern of stimuli. We tested conditions viewing natural images through actual foggy filters as well as simulated images, using a colorfulness matching method. Observers memorized the colorfulness of a stimulus image without foggy filters. Then they adjusted the colorfulness of a natural image through foggy ...
Calorie restriction has such a strong effect on health and longevity in laboratory animals that any study failing to account for it - which is pretty much everything run prior to the mid 1990s - is potentially tainted. You think your treatment is providing benefits? No, it just makes the mice feel unwell, and so they eat less. Similarly, within the realm of deliberate calorie restriction studies, those that fail to correctly control feeding are probably producing incorrect results. No-one said that science was easy, and fly studies - where liquid foods are used - are particularly troublesome: "Recent studies have indicated that flies respond to dilute food solutions by compensatory feeding. The existence of compensation mechanisms calls for a reconsideration of the relationships between diet, feeding behaviour and longevity. This study shows that flies fed on liquid diets, sense sucrose and yeast nutrients and adapt to changes in the quantity and presentation of the two nutrients. ... ...
An Interferometric Modulator (IMod) is a microelectromechanical device for modulating light using interference. The colors of these devices may be determined in a spatial fashion, and their inherent color shift may be compensated for using several optical compensation mechanisms. Brightness, addressing, and driving of IMods may be accomplished in a variety of ways with appropriate packaging, and peripheral electronics which can be attached and/or fabricated using one of many techniques. The devices may be used in both embedded and directly perceived applications, the latter providing multiple viewing modes as well as a multitude of product concepts ranging in size from microscopic to architectural in scope.
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This section has an overview and detailed reference pages on making. UNet Models and Notebooks for Industrial Quality Inspection The UNet model is a convolutional auto-encoder for 2D image segmentation used in industrial quality inspection. Before going forward you should read the paper entirely at least once. Anybody, please, can you give me some link or code for player movement interpolation and latency compensation on Unity 5. They apply simulated force to a known mesh and generate the desired. We interpret a video CNN as a collection of multi-stream space. It helps in visualizing data. The model is build from the keras library from python, which provides many useful class to construct the 3D unet model. NVIDIA contributed 10 variations of UNet to TensorFlow Hub with notebooks to try, each specializing in detecting different defects (eg: scratches, spots, etc. Thanks again for your valuable contributions to the community. GitHub Gist: instantly share code, notes, and snippets. The ports and ...
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I just know how Sundown is with the RMS rateings... wanna give it all she can take without getting Hot. Want her to last long too... was thinking 2000...
Steps to reproduce: 1. Download and import attached project. EDIT: (CurvesSpace.zip) 2. Open scene: main 3. Select and simulate part...
The contrasting dose of sex chromosomes in males and females potentially introduces a large-scale imbalance in levels of gene expression between sexes, and between sex chromosomes and autosomes. In many organisms, dosage compensation has thus evolved to equalize sex-linked gene expression in males and females. In mammals this is achieved by X chromosome inactivation and in flies and worms by up- or down-regulation of X-linked expression, respectively. While otherwise widespread in systems with heteromorphic sex chromosomes, the case of dosage compensation in birds (males ZZ, females ZW) remains an unsolved enigma. Here, we use a microarray approach to show that male chicken embryos generally express higher levels of Z-linked genes than female birds, both in soma and in gonads. The distribution of male-to-female fold-change values for Z chromosome genes is wide and has a mean of 1.4-1.6, which is consistent with absence of dosage compensation and sex-specific feedback regulation of gene expression at
X monosomic mice (39,XO) have a remarkably mild phenotype when compared to women with Turner syndrome (45,XO). The generally accepted hypothesis to explain this discrepancy is that the number of genes on the mouse X chromosome which escape X inactivation, and thus are expressed at higher levels in females, is very small. However this hypothesis has never been tested and only a small number of genes have been assayed for their X-inactivation status in the mouse. We performed a global expression analysis in four somatic tissues (brain, liver, kidney and muscle) of adult 40,XX and 39,XO mice using the Illumina Mouse WG-6 v1_1 Expression BeadChip and an extensive validation by quantitative real time PCR, in order to identify which genes are expressed from both X chromosomes. We identified several genes on the X chromosome which are overexpressed in XX females, including those previously reported as escaping X inactivation, as well as new candidates. However, the results obtained by microarray and qPCR were
Female mammals inactivate one of the two X chromosomes in each somatic cell in order to balance the X-linked gene dosage between females and males (X chromosome inactivation, XCI). This process is mediated by non-coding RNA X inactive specific transcript (Xist). Here, I show that, when embryonic stem (ES) cells were cultured under undifferentiated condition, inducible Xist was sufficient to silence genes in vitro. Furthermore, the induced XCI was counteracted by the endogenous capability of X chromosome reactivation (XCR) in the pluripotent ES cells. Thus, perturbing XCR players should tip the balance towards stronger gene silencing effects. Using this experimental system, we show that shRNA knock- down of histone acetyltransferase Kat8 and its associated protein from Male Specific Lethal (MSL) complex, Msl2, significantly enhanced the gene silencing effect of induced XCI in undifferentiated ES cells. Interestingly, Kat8 and Msl2 are involved in Drosophila dosage compensation by up-regulating ...
X-inactivation (also called lyonization) is a process by which one of the copies of the X chromosome present in female mammals is inactivated. The inactive X chromosome is silenced by its being packaged in such a way that it has a transcriptionally inactive structure called heterochromatin. As nearly all female mammals have two X chromosomes, X-inactivation prevents them from having twice as many X chromosome gene products as males, who only possess a single copy of the X chromosome (see dosage compensation). The choice of which X chromosome will be inactivated is random in placental mammals such as humans, but once an X chromosome is inactivated it will remain inactive throughout the lifetime of the cell and its descendants in the organism. Unlike the random X-inactivation in placental mammals, inactivation in marsupials applies exclusively to the paternally derived X chromosome. In 1959 Susumu Ohno showed that the two X-chromosomes of mammals were different: one appeared similar to the ...
Video created by The University of Melbourne for the course Epigenetic Control of Gene Expression. X chromosome inactivation is a really well-characterised epigenetic process that is now used as a model system to study epigenetic processes that ...
Thursday 7 April 2011 X chromosome-inactivation -- a crucial genetic balancing mechanism that occurs in all females - is not as balanced as previously thought, with a new study adding further evidence to the case.. Researchers from the Institute of Psychiatry and colleagues found evidence that gene inactivation is often skewed toward one X chromosome over the other, and that this bias may already be established in early childhood. The findings add to our understanding of the factors influencing sex differences, and how that may affect complex diseases. Despite the overall high similarity in X chromosome inactivation patterns in identical twins at both ages 5 and 10 years, some identical twin-pairs had noticeably different patterns. This adds to the growing body of evidence showing how genetically identical individuals can be different in the way their genes are expressed. The differences in X chromosome inactivation between genetically identical twins highlight the potential relevance of skewed ...
Limitations: Testing is limited to XX females only. This assay will be uninformative in up to 20 percent of females due to homozygosity for the polymorphic AR gene locus analyzed. XCI patterns may differ among tissues; therefore, the XCI ratio reported is for the tissue type tested with a standard deviation 0.09 in random XCI; 0.06 in non-random XCI. Although this test will detect the methylation status of the X-chromosomes, it will not determine if the X inactivation pattern is associated with rearrangements of the X chromosome, pathogenic variants in X-linked genes or neoplastic disease. If a non-random XCI pattern is present, the parent of origin of the active X cannot be determined without testing parental samples. XCI ratios should not be used to predict prognosis for female carriers of X-linked disorders as variable expressivity may result due to other genetic or environmental modifiers. Because the level of XCI may differ in prenatal specimens and whole blood, this test is not recommended ...
73 year old female with choroideremia (carrier). She has her father with choroideremia. She has noticed distortion in the right eye for 4 months. She had never been told her retinas were abnormal. VA 20/80 OD, 20/32 OS. ...
POSTER 50 - CHROMATIN DOMAINS THAT ESCAPE X INACTIVATION CHARACTERIZED BY CTCF BINDING AND HISTONE MODIFICATIONS Cheng MK 1, Filippova GN 2, Disteche CM 1 1 University of Washington, Seattle, United States, 2 Fred Hutchinson Cancer Research Center, Seattle, United States Genes that escape X inactivation are expressed in the context of inactive chromatin and must therefore employ some mechanism to overcome the repressive structure of the inactive X chromosome. One possible mechanism is binding of the chromatin insulator CTCF, which we hypothesize, acts as a boundary element between inactivated and escape regions on the X. We have found CTCF binding sites at the 5 CpG islands of Jarid1c and Eif2s3x, two mouse genes that escape X inactivation and are adjacent to an inactivated gene. We have also shown that DNA methylation is very low at the CpG island of Jarid1c. To characterize the chromatin structure of transition regions, we are using chromatin immunoprecipitation and real-time PCR to map the ...
In healthy women with to normal X-chromosomes, the one of the X-chromosomes is switched off (silenced). The X-chromosome which is silenced varies from cell to cell. The silencing is controlled by a part of the X-chromosome designated XIC (X-inactivation center). The inactivation/silencing of the X-chromosome is initiated by a gene named Xist-gene (the X inactivation specific transcript).This gene encodes specific structures so called lincRNAs (long intervening specific transcripts) which are very similar to our genetic material (DNA) but which is not coding for proteins. The final result is that women are X-chromosome mosaics with one X-chromosome from the mother and the other X from the father. However, numerous genes on the X-chromosome escape this silencing process by an unknown mechanism. Approximately two third of the genes are silenced, 15 % avoid silencing and 20 percent are silenced or escape depending on the tissue of origin.. The aforementioned long non-protein-coding parts of our ...
Coordinate gene regulation is a fundamental process essential to all cells from the germ line to the immune system. Our long-term goal is to define how genes are identified for coordinate regulation, the key initial step in their regulation. Dosage compensation is one of the best model systems for studying this process because all of the genes on a single chromosome are specifically identified and co-regulated. Drosophila, like mammals, increase the transcript levels of a large number of diversely-regulated genes along the length of the single male X-chromosome precisely two-fold relative to each female X-chromosome.. We are developing innovative approaches to understanding how dosage compensation in Drosophila is established, the critical first step in coordinate regulation. In this way, we will address the following key overall question: How are global and gene-specific transcriptional regulatory signals integrated to precisely regulate genes? By combining genetic, biochemical, and genomic ...
Down syndrome (DS) is a common disorder with enormous medical and social costs, caused by trisomy for chromosome 21 (Chr21). We tested the concept that gene imbalance across an extra chromosome can be de facto corrected by manipulating a single gene, XIST. Using genome editing with zinc finger nucleases, we targeted a large, inducible XIST transgene into the Chr21 DYRK1A locus, in DS pluripotent stem cells. XIST RNA coats Chr21 and triggers stable heterochromatin modifications, chromosome-wide transcriptional silencing and DNA methylation to form a
What is a Barr body? Barr body is an inactive X-chromosome found in a female somatic cell. The phenomenon of X inactivation or dosage compensation was originally described by Mary Lyon and is also known as lyonization or Lyon law.
For a long time it was assumed that the heart did not have enough power to pump in the case of cardiac insufficiency. But it is not only the strength that the weak heart lacks. In the course of the cardiac insufficiency, the heart also changes - it enlarges and "wears out". The reason for the change is that due to the lower pumping force, the heart has to exert itself over a longer period of time in order to transport sufficient blood through the body. This is an additional strain on the organism. Since the heart is a muscle, it tries to compensate for the higher effort by increasing muscle formation. The heart becomes both heavier and stiffer and less elastic.. The result: the blood supply to the heart and the body deteriorates continuously. The resulting lack of oxygen means great stress for the body and its organs. It therefore reacts with various measures to maintain normal bodily functions as far as possible. So-called compensation mechanisms ensure normal blood circulation for some time, ...
My laboratory studies the X-chromosome inactivation (XCI) process. This process leads to one transcriptionally inactive X chromosome in every female mammalian cell, required to compensate for dosage differences of X encoded genes between male and female cells. Our research focus is aimed at the identification and characterization of mechanisms directing female specific initiation of XCI, and epigenetic mechanisms involved in the silencing process.. Keywords: X inactivation / transcription factors / stochastics / early mammalian development / Rnf12. Subject area(s): Chromatin & Transcription , Development , Genome Stability & Dynamics. ...
Mario, In principle I agree with you that the computer is more accurate in performing compensations on the more complex experiments. I am merely asking this so you can put everyones (at least my) first question at ease. Are the computers always right? Have you found any potential bugs in the system where the computer (and I am not assuming any particular software) is incorrect because of some unforseen influences in the input data? I know this is vague, but while I trust in the programmers abilities, you are actually doing the most complex experiments with more colors and may have found some caveats for which we must all be aware. Randy T. Fischer NIH/NIAMS Building 10, Room 6D57 9000 Rockville Pike Bethesda, MD 20892 (301) 594-3537 fischer1 at mail.nih.gov , ---------- , From: Mario Roederer , Sent: Friday, June 14, 2002 5:42 PM , To: Cytometry Mailing List , Subject: Re: newbie help with software compensation , , , (OK, whos surprised that it took me this long to weigh in?) , , David ...
The effects of monetary compensation on performance are often debated. One of the most popular theories on the subject is psychologist Frank Herzbergs Two-Factor Theory. Somewhat derived from Maslows Hierarchy of Needs, Herzbergs theory indicates that while pay is a demotivating factor if not adequate for the work, ...
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X-chromosome (Barr body) - posted in Cell Biology: Hi everybody! I want to know what specific staining procedure is used to demonstrate the X-chromosomes or Barr bodies in cells. Is there a protocol for this? If you have or hapen to know one please send me a copy, thank you very much.