Points of comparison : what indicating gestures tell us about the origins of signs in San Juan Quiahije Chatino sign language

New languages emerge under rare conditions, when deaf children who cannot access the vocal-auditory language(s) used around them invent visual-manual communication systems of their own. Such homesign or family sign systems have simple structures but nevertheless show the hallmarks of language, including a stable lexicon of signs composed of meaningful, recombinable elements. Prior research has found that many of these elements are invented by signers, though some are adapted from the gestural input received from hearing interlocutors. The current project returns to this claim, examining the influence of gestures on the structure of two emerging family sign languages used in a rural, indigenous community in Oaxaca, Mexico. It focuses on foundational, visually accessible ‘indicating gestures’ such as pointing that direct the addressees attention to a region in physical space. Three linked studies were performed to investigate whether indicating gestures have internal structure that is accessible to deaf signers, and whether such structure is incorporated into their emerging languages. In the first, the spontaneous, speech-linked indicating gestures of hearing people were examined for internal structure. They were found to comprise three recombinable elements that, through systematic modulations in form, convey information about the direction and distance of targets. A second study looked for a relationship between the form of indicating gestures and the features of the speech that accompanies them. No such relationship was found, suggesting that the meaningful modulation of the gesture features occurs independently from speech. The final study compared the forms and meanings of two deaf signers’ indicating gestures with those of the hearing participants. Signers were found to use the direction and elbow height features, but not the handshape features, from the conventional indicating system. These findings reveal that indicating gestures, often described as holistic, non-composite signals, in fact exhibit an internal structure that can be incorporated into an emerging signed language. Interestingly, they also reveal that not all features of gestures—even ones that exhibit clear patterning—will be adopted by signers, perhaps because gesture features must be both systematically patterned and visually iconic for signers to interpret them as meaningful.Linguistic

Fractional Hardy-Sobolev type inequalities for half spaces and John domains

As our main result we prove a variant of the fractional Hardy-Sobolev-Maz'ya inequality for half spaces. This result contains a complete answer to a recent open question by Musina and Nazarov. In the proof we apply a new version of the fractional Hardy-Sobolev inequality that we establish also for more general unbounded John domains than half spaces

Placing Mercy in Hume's Catalogue of Moral Virtues

(Statement of Responsibility) by Kathryn Mesh Iserman(Thesis) Thesis (B.A.) -- New College of Florida, 2006(Electronic Access) RESTRICTED TO NCF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE(Bibliography) Includes bibliographical references.(Source of Description) This bibliographic record is available under the Creative Commons CC0 public domain dedication. The New College of Florida, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.(Local) Faculty Sponsor: Langston, Dougla

Vitamin C Induces Specific Demethylation of H3K9me2 in Mouse Embryonic Stem Cells via Kdm3a/b

Histone methylation patterns regulate gene expression and are highly dynamic during development. The erasure of histone methylation is carried out by histone demethylase enzymes. We had previously shown that vitamin C enhances the activity of Tet enzymes in embryonic stem (ES) cells, leading to DNA demethylation and activation of germline genes. We report here that vitamin C induces a remarkably specific demethylation of histone H3 lysine 9 dimethylation (H3K9me2) in ES cells. Vitamin C treatment reduces global levels of H3K9me2, but not other histone methylation marks analyzed, as measured by western blot, immunofluorescence and mass spectrometry. Vitamin C leads to widespread loss of H3K9me2 at large chromosomal domains as well as gene promoters and repeat elements. Vitamin C-induced loss of H3K9me2 occurs rapidly within 24 hours and is reversible. Importantly, we found that the histone demethylases Kdm3a and Kdm3b are required for vitamin C-induced demethylation of H3K9me2. Moreover, we show that vitamin C-induced Kdm3a/b-mediated H3K9me2 demethylation and Tet-mediated DNA demethylation are independent processes. Lastly, we document Kdm3a/b are partially required for the up-regulation of germline genes by vitamin C. These results reveal a specific role for vitamin C in histone demethylation in ES cells, and document that DNA methylation and H3K9me2 cooperate to silence germline genes in pluripotent cells

Vitamin C induces specific demethylation of H3K9me2 in mouse embryonic stem cells via Kdm3a/b

Background: Histone methylation patterns regulate gene expression and are highly dynamic during development. The erasure of histone methylation is carried out by histone demethylase enzymes. We had previously shown that vitamin C enhances the activity of Tet enzymes in embryonic stem (ES) cells, leading to DNA demethylation and activation of germline genes. Results: We report here that vitamin C induces a remarkably specific demethylation of histone H3 lysine 9 dimethylation (H3K9me2) in naïve ES cells. Vitamin C treatment reduces global levels of H3K9me2, but not other histone methylation marks analyzed, as measured by western blot, immunofluorescence and mass spectrometry. Vitamin C leads to widespread loss of H3K9me2 at large chromosomal domains as well as gene promoters and repeat elements. Vitamin C-induced loss of H3K9me2 occurs rapidly within 24 h and is reversible. Importantly, we found that the histone demethylases Kdm3a and Kdm3b are required for vitamin C-induced demethylation of H3K9me2. Moreover, we show that vitamin C-induced Kdm3a/b-mediated H3K9me2 demethylation and Tet-mediated DNA demethylation are independent processes at specific loci. Lastly, we document Kdm3a/b are partially required for the upregulation of germline genes by vitamin C. Conclusions: These results reveal a specific role for vitamin C in histone demethylation in ES cells and document that DNA methylation and H3K9me2 cooperate to silence germline genes in pluripotent cells.Science, Faculty ofOther UBCNon UBCMicrobiology and Immunology, Department ofReviewedFacult

Maternal vitamin C regulates reprogramming of DNA methylation and germline development

Development is often assumed to be hardwired in the genome, but several lines of evidence indicate that it is susceptible to environmental modulation with potential long-term consequences, including in mammals1,2. The embryonic germline is of particular interest because of the potential for intergenerational epigenetic effects. The mammalian germline undergoes extensive DNA demethylation3–7 that occurs in large part by passive dilution of methylation over successive cell divisions, accompanied by active DNA demethylation by TET enzymes3,8–10. TET activity has been shown to be modulated by nutrients and metabolites, such as vitamin C11–15. Here we show that maternal vitamin C is required for proper DNA demethylation and the development of female fetal germ cells in a mouse model. Maternal vitamin C deficiency does not affect overall embryonic development but leads to reduced numbers of germ cells, delayed meiosis and reduced fecundity in adult offspring. The transcriptome of germ cells from vitamin-C-deficient embryos is remarkably similar to that of embryos carrying a null mutation in Tet1. Vitamin C deficiency leads to an aberrant DNA methylation profile that includes incomplete demethylation of key regulators of meiosis and transposable elements. These findings reveal that deficiency in vitamin C during gestation partially recapitulates loss of TET1, and provide a potential intergenerational mechanism for adjusting fecundity to environmental conditions.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Maternal vitamin C regulates reprogramming of DNA methylation and germline development

Development is often assumed to be hardwired in the genome, but several lines of evidence indicate that it is susceptible to environmental modulation with potential long-term consequences, including in mammals1,2. The embryonic germline is of particular interest because of the potential for intergenerational epigenetic effects. The mammalian germline undergoes extensive DNA demethylation3-7 that occurs in large part by passive dilution of methylation over successive cell divisions, accompanied by active DNA demethylation by TET enzymes3,8-10. TET activity has been shown to be modulated by nutrients and metabolites, such as vitamin C11-15. Here we show that maternal vitamin C is required for proper DNA demethylation and the development of female fetal germ cells in a mouse model. Maternal vitamin C deficiency does not affect overall embryonic development but leads to reduced numbers of germ cells, delayed meiosis and reduced fecundity in adult offspring. The transcriptome of germ cells from vitamin-C-deficient embryos is remarkably similar to that of embryos carrying a null mutation in Tet1. Vitamin C deficiency leads to an aberrant DNA methylation profile that includes incomplete demethylation of key regulators of meiosis and transposable elements. These findings reveal that deficiency in vitamin C during gestation partially recapitulates loss of TET1, and provide a potential intergenerational mechanism for adjusting fecundity to environmental conditions

MOESM1 of Vitamin C induces specific demethylation of H3K9me2 in mouse embryonic stem cells via Kdm3a/b

Additional file 1: Figure S1. Evaluation of changes in H3 PTMs following vitamin C treatment. A) Western blot for several H3 PTMs in ES cells ± vitamin C. B) Immunofluorescence for H3K9me2 and corresponding DAPI staining in untreated and vitamin C-treated ES cells. Merged images show H3K9me2 in green and DAPI staining in red. H3K9me2 immunofluorescence is also shown in Fig. 1e. Scale bar represents 20 μm

MOESM4 of Vitamin C induces specific demethylation of H3K9me2 in mouse embryonic stem cells via Kdm3a/b

Additional file 4: Figure S4. Analysis of H3K9me2 at repetitive elements in ES cells treated with vitamin C. ChIP-qPCR for H3K9me2 in ES cells ± vitamin C at the repetitive element families indicated. ChIP for IgG was performed as a negative control. Data are mean ± SD. Asterisks represent P < 0.05 by t test

MOESM2 of Vitamin C induces specific demethylation of H3K9me2 in mouse embryonic stem cells via Kdm3a/b

Additional file 2: Figure S2. Analysis of H3K9me2 in G9a and GLP knockout ES cells treated with vitamin C. A) Western blot for H3K9me2 in wild-type parental TT2, G9a knockout, and GLP knockout ES cells ± vitamin C. B) Immunofluorescence for H3K9me2 in GiP ES cells ± vitamin C and untreated wild-type TT2, G9a knockout, and GLP knockout ES cells. GiP ES cells treated with vitamin C show a H3K9me2 staining pattern that is similar to G9a and GLP knockout ES cells. Scale bar represents 20 μm