RESUMO
Recent attempts at the construction of holography for asymptotically flat spacetime have taken two different routes. Celestial holography, involving a two dimensional (2D) conformal field theory (CFT) dual to 4D Minkowski spacetime, has generated novel results in asymptotic symmetry and scattering amplitudes. A different formulation, using Carrollian CFTs, has been principally used to provide some evidence for flat holography in lower dimensions. Understanding of flat space scattering has been lacking in the Carroll framework. In this Letter, using ideas from Celestial holography, we show that 3D Carrollian CFTs living on the null boundary of 4D flat space can potentially compute bulk scattering amplitudes. Three-dimensional Carrollian conformal correlators have two different branches, one depending on the null time direction and one independent of it. We propose that it is the time-dependent branch that is related to bulk scattering. We construct an explicit field theoretic example of a free massless Carrollian scalar that realizes some desired properties.
RESUMO
Epithelial cells exhibit apical membrane protrusions, which confer specific functions to epithelial tissues. Microridges are short actin protrusions that are laterally long and form a maze-like pattern in the apical domain. They are widely found on vertebrate squamous epithelia including epidermis and have functions in mucous retention, membrane storage and abrasion resistance. It is largely unknown how the formation of these laterally long actin projections is regulated. Here, we show that antagonistic interactions between aPKC and Lgl-regulators of apical and basolateral domain identity, respectively,-control the length of microridges in the zebrafish periderm, the outermost layer of the epidermis. aPKC regulates the levels of Lgl and the active form of non-muscle myosinII at the apical cortex to prevent actin polymerization-dependent precocious fusion and elongation of microridges. Our data unravels the functional significance of exclusion of Lgl from the apical domain in epithelial cells.
Assuntos
Epiderme/metabolismo , Células Epiteliais/metabolismo , Glicoproteínas/metabolismo , Proteína Quinase C/metabolismo , Proteínas de Peixe-Zebra/metabolismo , Peixe-Zebra/genética , Citoesqueleto de Actina/genética , Citoesqueleto de Actina/metabolismo , Citoesqueleto de Actina/ultraestrutura , Actinas/genética , Actinas/metabolismo , Animais , Animais Geneticamente Modificados , Polaridade Celular , Embrião não Mamífero , Desenvolvimento Embrionário/genética , Células Epidérmicas , Epiderme/crescimento & desenvolvimento , Células Epiteliais/ultraestrutura , Regulação da Expressão Gênica no Desenvolvimento , Glicoproteínas/antagonistas & inibidores , Glicoproteínas/genética , Morfolinos/genética , Morfolinos/metabolismo , Miosina Tipo II/genética , Miosina Tipo II/metabolismo , Proteína Quinase C/genética , Peixe-Zebra/crescimento & desenvolvimento , Peixe-Zebra/metabolismo , Proteínas de Peixe-Zebra/antagonistas & inibidores , Proteínas de Peixe-Zebra/genéticaRESUMO
The epidermis is a stratified epithelium, which forms a barrier to maintain the internal milieu in metazoans. Being the outermost tissue, growth of the epidermis has to be strictly coordinated with the growth of the embryo. The key parameters that determine tissue growth are cell number and cell size. So far, it has remained unclear how the size of epidermal cells is maintained and whether it contributes towards epidermal homeostasis. We have used genetic analysis in combination with cellular imaging to show that zebrafish goosepimples/myosin Vb regulates plasma membrane homeostasis and is involved in maintenance of cell size in the periderm, the outermost epidermal layer. The decrease in peridermal cell size in Myosin Vb deficient embryos is compensated by an increase in cell number whereas decrease in cell number results in the expansion of peridermal cells, which requires myosin Vb (myoVb) function. Inhibition of cell proliferation as well as cell size expansion results in increased lethality in larval stages suggesting that this two-way compensatory mechanism is essential for growing larvae. Our analyses unravel the importance of Myosin Vb dependent cell size regulation in epidermal homeostasis and demonstrate that the epidermis has the ability to maintain a dynamic balance between cell size and cell number.
Assuntos
Membrana Celular/metabolismo , Células Epidérmicas , Epiderme/metabolismo , Homeostase , Miosina Tipo V/metabolismo , Animais , Contagem de Células , Tamanho Celular , Embrião não Mamífero , Endocitose , Endossomos/metabolismo , Epiderme/embriologia , Loci Gênicos , Lisossomos/metabolismo , Modelos Biológicos , Mutação , Miosina Tipo V/deficiência , Miosina Tipo V/genética , Fenótipo , Peixe-ZebraRESUMO
Mitochondrial morphology is regulated by conserved proteins involved in fusion and fission processes. The mammalian Optic atrophy 1 (OPA1) that functions in mitochondrial fusion is associated with Optic Atrophy and has been implicated in inner membrane cristae remodeling during cell death. Here, we show Drosophila Optic atrophy 1-like (Opa1-like) influences mitochondrial morphology through interaction with 'mitochondria-shaping' proteins like Mitochondrial assembly regulatory factor (Marf) and Drosophila Mitofilin (dMitofilin). To gain an insight into Opa1-like's network, we delineated bonafide interactors like dMitofilin, Marf, Serine protease High temperature requirement protein A2 (HTRA2), Rhomboid-7 (Rho-7) along with novel interactors such as Mortalin ortholog (Hsc70-5) from Drosophila mitochondrial extract. Interestingly, RNAi mediated down-regulation of hsc70-5 in Drosophila wing imaginal disc's peripodial cells resulted in fragmented mitochondria with reduced membrane potential leading to proteolysis of Opa1-like. Increased ecdysone activity induced dysfunctional fragmented mitochondria for clearance through lysosomes, an effect enhanced in hsc70-5 RNAi leading to increased cell death. Over-expression of Opa1-like rescues mitochondrial morphology and cell death in prepupal tissues expressing hsc70-5 RNAi. Taken together, we have identified a novel interaction between Hsc70-5/Mortalin and Opa1-like that influences cellular homeostasis through mitochondrial fusion.
Assuntos
Proteínas de Drosophila/metabolismo , Drosophila melanogaster/metabolismo , Proteínas de Choque Térmico HSC70/metabolismo , Proteínas de Choque Térmico HSP70/metabolismo , Homeostase/fisiologia , Proteínas de Membrana/metabolismo , Proteínas Mitocondriais/metabolismo , Proteômica/métodos , Animais , Apoptose , Western Blotting , Diferenciação Celular , Proliferação de Células , Células Cultivadas , Proteínas de Drosophila/genética , Drosophila melanogaster/genética , Drosophila melanogaster/crescimento & desenvolvimento , Regulação da Expressão Gênica no Desenvolvimento , Proteínas de Choque Térmico HSC70/genética , Proteínas de Choque Térmico HSP70/genética , Hemócitos/metabolismo , Técnicas Imunoenzimáticas , Imunoprecipitação , Larva/genética , Larva/crescimento & desenvolvimento , Larva/metabolismo , Potencial da Membrana Mitocondrial , Proteínas de Membrana/genética , Mitocôndrias/química , Mitocôndrias/metabolismo , Proteínas Mitocondriais/genética , RNA Mensageiro/genética , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por MatrizRESUMO
In this Letter, we consider the variation of the entanglement entropy of a region as the shape of the entangling surface is changed. We show that the variation satisfies a Wess-Zumino-like integrability condition in field theories which can be consistently coupled to gravity. In this case, the "anomaly" is localized on the entangling surface. The solution of the integrability condition should give all the nontrivial finite local terms which can appear in the variation of the entanglement entropy. The answers depend on the intrinsic and extrinsic geometry of the entangling surface, but the form does not depend on the details of the field theory. The coefficients, which multiply the purely geometric contributions, will depend on the particular details of the field theory.
RESUMO
We construct a quantum mechanical perturbation theory which uses the multiple time scale technique. Working with the time translation operator, we use a variant on the method of Bender and Bettencourt. Our perturbation theory smoothly crosses over to the classical result as Planck's -->0. It is seen that this technique has a nonperturbative element built into it.