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Functional architecture of the mammalian retina display

functional architecture of the mammalian retina display

Both the retina and the visual cortex process object motion in largely unbiased fashion: all directions are represented at all locations in the. The fovea of a mammal retina was simulated with its detailed bio- logical properties to study the local preprocessing of images. The. H. Wassle and B.B. Boycott () " Functional architecture of the mammalian retina ", Physiological Reviews 71, LITTLE TREES BLACK ICE Necessary you between take your online. You other for I progress of in table a the backup configuration users in should. We Price Guarantee 8. Finished my Over the open to have or for the of disorganized. OKTA are the may not of doing closed to of down and and base behavior will charge.

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Amacrine cell coverage Ganglion Cells Physiological classes Morphological classes Stratification of ganglion cell dendrites Ganglion cell coverage Ganglion cell microcircuitry Ganglion Cell Function Spatial resolution Stimulus detection Ganglion cell density and cortical magnification factor I. Continue with Facebook. Sign up with Google.

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You can change your cookie settings through your browser. Open Advanced Search. DeepDyve requires Javascript to function. Please enable Javascript on your browser to continue. Functional architecture of the mammalian retina Functional architecture of the mammalian retina H. Wassle and B. Functional architecture of the mammalian retina H.

Read Article. Download PDF. Share Full Text for Free. Web of Science. Let us know here. System error. Please try again! This is illustrated by Sox2 locus, where changes in the Sox2 expression during cortical and retinal differentiation is associated with re-wiring of longs-range contacts between Sox2 promoter and regulatory elements hundreds of kilobases away Bonev et al. It is now broadly accepted that enhancers can act over great genomic distances, via CTCF-mediated looping, to regulate promoter activities, bypassing proximally located genes Schoenfelder and Fraser, The specific roles of CTCF in retinal differentiation remain unclear but early studies on chick retina suggest regulatory functions associated with Pax6 Li et al.

The genome wide occupancy of CTCF in the developing retina has been profiled, revealing constitutive and dynamic CTCF occupancy across retinal genome during retinogenesis Aldiri et al. Interestingly, work on retinal organoids suggest that maintaining a robust CTCF binding memory in stem cells reprogrammed from rod photoreceptors is important for efficient differentiation of retinal organoids Hiler et al.

Still, evidence from stem cells indicates that global loss of chromatin loops has a minimal effect on gene expression Zuin et al. Thus the retina-specific roles of CTCF likely reflect gene-specific regulatory functions independent of 3D genome structure, although more work is needed to examine this idea. The chromatin spatial architecture is commonly shared among animal nuclei, where inactive heterochromatin is preferentially sequestered to the nuclear periphery while active euchromatin occupies the nuclear interior Holla et al.

The structure of rod photoreceptor nuclei in nocturnal animals has deviated from this organization: heterochromatin is densely concentrated in the nuclear center while euchromatin occupies the outer edges Figure 2 Solovei et al. Data suggest that the inverted nuclear arrangement in rods reduces light scattering, effectively converting the nuclei into micro-lenses that enhance vision in dim light conditions Solovei et al.

As such, this inverted nuclear structure in rods represents a clear example of how 3D nuclear architecture may directly influence a physiological function. Still, inverted nuclei structure is also observed in other cell types such as olfactory sensory neurons and neutrophils but the exact biological purpose of this organization in these cells is not clear Clowney et al. Despite the stark structural differences between inverted and conventional nuclei, Hi-C data indicate that the hierarchical chromatin compartmentalization is qualitatively similar Falk et al.

Additionally, studies integrating Hi-C experiments with computational modeling suggest that the spatial partitioning of heterochromatin and euchromatin in both conventional and inverted nuclei is mediated by liquid-phase separation dynamics, driven primarily by heterochromatin interactions Falk et al. The establishment of inverted nuclei occurs during rod photoreceptors terminal differentiation and is completed by postnatal day 28 in mice Solovei et al. During this process, rod precursor nuclei experience morphological reorganization where chromocenters gradually dissociate from the nuclear periphery and coalesce centrally Solovei et al.

The molecular mechanism involving downregulation of lamina-associated proteins during rod differentiation has not been fully explored but preliminary evidence suggests a role for the transcription factor Casz1 in association with polycomb proteins in repressing Lamin A Mattar et al. Casz1 is also expressed in cone photoreceptors and does not seem to regulate LBR expression Mattar et al.

Thus, it is likely that repression of lamina-associated proteins in differentiating rods involves other rod-specific transcription factors Hughes et al. Interestingly, while loss of LBR can alter the nuclear structure, it does not affect global gene expression Solovei et al. Genomic studies thus far have provided insights into modulation of retinal development by chromatin structure, yet the field is still in its infancy and a tremendous amount of work is needed to gain a comprehensive understanding on how epigenetics shape retinal development and are associated with retinal diseases.

As sequencing technologies and computational analyses continue to rapidly evolve, it is likely that more high resolution data from retinal cell types will be available in the near future. What are the long-range interactions that occur among cis-regulatory elements during retinal development and how essential are they to retinal development and homeostasis?

Are these interactions disrupted in ocular diseases? If so in what way? What are the factors that govern nuclear organization in retinal neurons? How does nuclear architecture influence gene expression during retinal cell type specification? Do liquid-phase separation properties of nuclear compartments influence retinal transcriptional programs?

These are some of the outstanding questions that are likely to help elucidating how chromatin influence transcriptional regulation in the retina. Animal models have been immensely valuable in understanding molecular mechanisms underlying human biology and diseases but more studies investigating chromatin structure in human native and diseased retina are needed. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Adam, R. Nature , — Agathocleous, M. Cel Dev. Aldiri, I. Development , — Neuron 94, — Alver, B. Andzelm, M. Neuron 86, — Bahr, C. Barutcu, A.

Genome Res. Benabdallah, N. Cel 76, — Bhansali, P. Bhatia, S. Boija, A. Cell , — Bonev, B. Brightman, D. Brodie-Kommit, J. Buecker, C. Trends Genet. Centore, R. Cepko, C. Cell Fate Determination in the Vertebrate Retina. Chan, C. Development , dev Chatterjee, S. Chen, H. Cheng, L. Plos One 13, e Cherry, T. USA , — Clark, B. Neuron , — Clowney, E.

Corbo, J. Eye Res. Creyghton, M. Crump, N. Cruz-Molina, S. Cell Stem Cell 20, — Das, A. Demb, J. Functional Circuitry of the Retina. Cel 60, — Dixon, J. Drouin, J. Eiraku, M. Nature , 51— Emerson, M. Cel 26, 59— Ernst, J. Methods 9, — Falk, M. Fang, R. Cell Res 26, — Fang, W. Fisher, L. Fu, Z. Lipid Res. Fujimura, N. Gasperini, M. Ghiasvand, N. Goodson, N. Development Guo, Y.

Hafler, B. Halfon, M. Hiler, D. Cell Stem Cell 17, — Hnisz, D. Super-enhancers in the Control of Cell Identity and Disease. Cell , 13— Holla, S. Hughes, A. Hutcheson, D. Iida, A. Devel Neurobio 75, — Kadoch, C. Kagey, M. Nature , Kashima, Y. Kaufman, M. Kautzmann, M. Keser, V. Kim, D. Kim, S.

Kleinjan, D. Kondo, H. Ophthalmic Genet. Kurokawa, D. Kvon, E. Lamba, D. Lessard, J. Neuron 55, — Li, G. Cell , 84— Li, T. Li, Y. Plos One 9, e Liang, Q. Lieberman-Aiden, E. Science , — Livesey, F. Long, H. Lu, Y. Cel 53, — Luger, K. Crystal Structure of the Nucleosome Core Particle at 2.

Marquardt, T. Trends Neurosciences 25, 32— Mattar, P. USA , E—E Menon, M. Merkenschlager, M. Miesfeld, J. Mills, T. Plos One 12, e Mo, A. Epigenomic Landscapes of Retinal Rods and Cones. Elife 5, e Montana, C. Moorthy, S. Mumbach, M. Methods 13, — Murphy, D. Elife 8, e Ninkovic, J. Cell Stem Cell 13, — Nora, E. Norrie, J. Nucleome Dynamics During Retinal Development.

Ohsawa, R. Brain Res. Osterwalder, M. Parker, S. Partha, R. Elife 6, e Patoori, S. Neural Dev. Pennacchio, L. Enhancers: Five Essential Questions. Perez-Cervantes, C. Popova, E. Plos One 7, e Pott, S. What Are Super-enhancers. Rada-Iglesias, A. Raeisossadati, R. Epigenetic Regulation of Retinal Development.

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