---
_id: '7033'
abstract:
- lang: eng
  text: Removal of the Bax gene from mice completely protects the somas of retinal
    ganglion cells (RGCs) from apoptosis following optic nerve injury. This makes
    BAX a promising therapeutic target to prevent neurodegeneration. In this study,
    Bax+/− mice were used to test the hypothesis that lowering the quantity of BAX
    in RGCs would delay apoptosis following optic nerve injury. RGCs were damaged
    by performing optic nerve crush (ONC) and then immunostaining for phospho-cJUN,
    and quantitative PCR were used to monitor the status of the BAX activation mechanism
    in the months following injury. The apoptotic susceptibility of injured cells
    was directly tested by virally introducing GFP-BAX into Bax−/− RGCs after injury.
    The competency of quiescent RGCs to reactivate their BAX activation mechanism
    was tested by intravitreal injection of the JNK pathway agonist, anisomycin. Twenty-four
    weeks after ONC, Bax+/− mice had significantly less cell loss in their RGC layer
    than Bax+/+ mice 3 weeks after ONC. Bax+/− and Bax+/+ RGCs exhibited similar patterns
    of nuclear phospho-cJUN accumulation immediately after ONC, which persisted in
    Bax+/− RGCs for up to 7 weeks before abating. The transcriptional activation of
    BAX-activating genes was similar in Bax+/− and Bax+/+ RGCs following ONC. Intriguingly,
    cells deactivated their BAX activation mechanism between 7 and 12 weeks after
    crush. Introduction of GFP-BAX into Bax−/− cells at 4 weeks after ONC showed that
    these cells had a nearly normal capacity to activate this protein, but this capacity
    was lost 8 weeks after crush. Collectively, these data suggest that 8–12 weeks
    after crush, damaged cells no longer displayed increased susceptibility to BAX
    activation relative to their naïve counterparts. In this same timeframe, retinal
    glial activation and the signaling of the pro-apoptotic JNK pathway also abated.
    Quiescent RGCs did not show a timely reactivation of their JNK pathway following
    intravitreal injection with anisomycin. These findings demonstrate that lowering
    the quantity of BAX in RGCs is neuroprotective after acute injury. Damaged RGCs
    enter a quiescent state months after injury and are no longer responsive to an
    apoptotic stimulus. Quiescent RGCs will require rejuvenation to reacquire functionality.
acknowledgement: This work was supported by National Eye Institute grants R01 EY012223
  (RWN), R01 EY030123 (RWN), T32 EY027721 (Department of Ophthalmology and Visual
  Sciences, University of Wisconsin-Madison), and a Vision Science Core grant P30
  EY016665 (Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison),
  an unrestricted funding grant from Research to Prevent Blindness (Department of
  Ophthalmology and Visual Sciences, University of Wisconsin-Madison), the Frederick
  A. Davis Endowment (RWN), and the Mr. and Mrs. George Taylor Foundation (RWN).
article_processing_charge: No
article_type: original
author:
- first_name: RJ
  full_name: Donahue, RJ
  last_name: Donahue
- first_name: Margaret E
  full_name: Maes, Margaret E
  id: 3838F452-F248-11E8-B48F-1D18A9856A87
  last_name: Maes
  orcid: 0000-0001-9642-1085
- first_name: JA
  full_name: Grosser, JA
  last_name: Grosser
- first_name: RW
  full_name: Nickells, RW
  last_name: Nickells
citation:
  ama: Donahue R, Maes ME, Grosser J, Nickells R. BAX-depleted retinal ganglion cells
    survive and become quiescent following optic nerve damage. <i>Molecular Neurobiology</i>.
    2020;57(2):1070–1084. doi:<a href="https://doi.org/10.1007/s12035-019-01783-7">10.1007/s12035-019-01783-7</a>
  apa: Donahue, R., Maes, M. E., Grosser, J., &#38; Nickells, R. (2020). BAX-depleted
    retinal ganglion cells survive and become quiescent following optic nerve damage.
    <i>Molecular Neurobiology</i>. Springer Nature. <a href="https://doi.org/10.1007/s12035-019-01783-7">https://doi.org/10.1007/s12035-019-01783-7</a>
  chicago: Donahue, RJ, Margaret E Maes, JA Grosser, and RW Nickells. “BAX-Depleted
    Retinal Ganglion Cells Survive and Become Quiescent Following Optic Nerve Damage.”
    <i>Molecular Neurobiology</i>. Springer Nature, 2020. <a href="https://doi.org/10.1007/s12035-019-01783-7">https://doi.org/10.1007/s12035-019-01783-7</a>.
  ieee: R. Donahue, M. E. Maes, J. Grosser, and R. Nickells, “BAX-depleted retinal
    ganglion cells survive and become quiescent following optic nerve damage,” <i>Molecular
    Neurobiology</i>, vol. 57, no. 2. Springer Nature, pp. 1070–1084, 2020.
  ista: Donahue R, Maes ME, Grosser J, Nickells R. 2020. BAX-depleted retinal ganglion
    cells survive and become quiescent following optic nerve damage. Molecular Neurobiology.
    57(2), 1070–1084.
  mla: Donahue, RJ, et al. “BAX-Depleted Retinal Ganglion Cells Survive and Become
    Quiescent Following Optic Nerve Damage.” <i>Molecular Neurobiology</i>, vol. 57,
    no. 2, Springer Nature, 2020, pp. 1070–1084, doi:<a href="https://doi.org/10.1007/s12035-019-01783-7">10.1007/s12035-019-01783-7</a>.
  short: R. Donahue, M.E. Maes, J. Grosser, R. Nickells, Molecular Neurobiology 57
    (2020) 1070–1084.
date_created: 2019-11-18T14:18:39Z
date_published: 2020-02-01T00:00:00Z
date_updated: 2023-08-17T14:05:48Z
day: '01'
department:
- _id: SaSi
doi: 10.1007/s12035-019-01783-7
external_id:
  isi:
  - '000493754200001'
  pmid:
  - '31673950'
intvolume: '        57'
isi: 1
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7035206/
month: '02'
oa: 1
oa_version: Submitted Version
page: 1070–1084
pmid: 1
publication: Molecular Neurobiology
publication_identifier:
  eissn:
  - 1559-1182
  issn:
  - 0893-7648
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: BAX-depleted retinal ganglion cells survive and become quiescent following
  optic nerve damage
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 57
year: '2020'
...
---
_id: '7369'
abstract:
- lang: eng
  text: Neuronal responses to complex stimuli and tasks can encompass a wide range
    of time scales. Understanding these responses requires measures that characterize
    how the information on these response patterns are represented across multiple
    temporal resolutions. In this paper we propose a metric – which we call multiscale
    relevance (MSR) – to capture the dynamical variability of the activity of single
    neurons across different time scales. The MSR is a non-parametric, fully featureless
    indicator in that it uses only the time stamps of the firing activity without
    resorting to any a priori covariate or invoking any specific structure in the
    tuning curve for neural activity. When applied to neural data from the mEC and
    from the ADn and PoS regions of freely-behaving rodents, we found that neurons
    having low MSR tend to have low mutual information and low firing sparsity across
    the correlates that are believed to be encoded by the region of the brain where
    the recordings were made. In addition, neurons with high MSR contain significant
    information on spatial navigation and allow to decode spatial position or head
    direction as efficiently as those neurons whose firing activity has high mutual
    information with the covariate to be decoded and significantly better than the
    set of neurons with high local variations in their interspike intervals. Given
    these results, we propose that the MSR can be used as a measure to rank and select
    neurons for their information content without the need to appeal to any a priori
    covariate.
acknowledgement: This research was supported by the Kavli Foundation and the Centre
  of Excellence scheme of the Research Council of Norway (Centre for Neural Computation).
  RJC is currently receiving funding from the European Union’s Horizon 2020 research
  and innovation programme under the Marie Skłodowska-Curie Grant Agreement No. 754411.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Ryan J
  full_name: Cubero, Ryan J
  id: 850B2E12-9CD4-11E9-837F-E719E6697425
  last_name: Cubero
  orcid: 0000-0003-0002-1867
- first_name: Matteo
  full_name: Marsili, Matteo
  last_name: Marsili
- first_name: Yasser
  full_name: Roudi, Yasser
  last_name: Roudi
citation:
  ama: Cubero RJ, Marsili M, Roudi Y. Multiscale relevance and informative encoding
    in neuronal spike trains. <i>Journal of Computational Neuroscience</i>. 2020;48:85-102.
    doi:<a href="https://doi.org/10.1007/s10827-020-00740-x">10.1007/s10827-020-00740-x</a>
  apa: Cubero, R. J., Marsili, M., &#38; Roudi, Y. (2020). Multiscale relevance and
    informative encoding in neuronal spike trains. <i>Journal of Computational Neuroscience</i>.
    Springer Nature. <a href="https://doi.org/10.1007/s10827-020-00740-x">https://doi.org/10.1007/s10827-020-00740-x</a>
  chicago: Cubero, Ryan J, Matteo Marsili, and Yasser Roudi. “Multiscale Relevance
    and Informative Encoding in Neuronal Spike Trains.” <i>Journal of Computational
    Neuroscience</i>. Springer Nature, 2020. <a href="https://doi.org/10.1007/s10827-020-00740-x">https://doi.org/10.1007/s10827-020-00740-x</a>.
  ieee: R. J. Cubero, M. Marsili, and Y. Roudi, “Multiscale relevance and informative
    encoding in neuronal spike trains,” <i>Journal of Computational Neuroscience</i>,
    vol. 48. Springer Nature, pp. 85–102, 2020.
  ista: Cubero RJ, Marsili M, Roudi Y. 2020. Multiscale relevance and informative
    encoding in neuronal spike trains. Journal of Computational Neuroscience. 48,
    85–102.
  mla: Cubero, Ryan J., et al. “Multiscale Relevance and Informative Encoding in Neuronal
    Spike Trains.” <i>Journal of Computational Neuroscience</i>, vol. 48, Springer
    Nature, 2020, pp. 85–102, doi:<a href="https://doi.org/10.1007/s10827-020-00740-x">10.1007/s10827-020-00740-x</a>.
  short: R.J. Cubero, M. Marsili, Y. Roudi, Journal of Computational Neuroscience
    48 (2020) 85–102.
date_created: 2020-01-28T10:34:00Z
date_published: 2020-02-01T00:00:00Z
date_updated: 2023-08-17T14:35:22Z
day: '01'
ddc:
- '004'
- '519'
- '570'
department:
- _id: SaSi
doi: 10.1007/s10827-020-00740-x
ec_funded: 1
external_id:
  isi:
  - '000515321800006'
file:
- access_level: open_access
  checksum: 036e9451d6cd0c190ad25791bf82393b
  content_type: application/pdf
  creator: rcubero
  date_created: 2020-01-28T09:31:09Z
  date_updated: 2020-07-14T12:47:56Z
  file_id: '7380'
  file_name: 10827_2020_740_MOESM1_ESM.pdf
  file_size: 1941355
  relation: supplementary_material
- access_level: open_access
  checksum: 4dd8b1fd4b54486f79d82ac7b2a412b2
  content_type: application/pdf
  creator: rcubero
  date_created: 2020-01-28T09:31:09Z
  date_updated: 2020-07-14T12:47:56Z
  file_id: '7381'
  file_name: Cubero2020_Article_MultiscaleRelevanceAndInformat.pdf
  file_size: 3257880
  relation: main_file
file_date_updated: 2020-07-14T12:47:56Z
has_accepted_license: '1'
intvolume: '        48'
isi: 1
keyword:
- Time series analysis
- Multiple time scale analysis
- Spike train data
- Information theory
- Bayesian decoding
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 85-102
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '754411'
  name: ISTplus - Postdoctoral Fellowships
publication: Journal of Computational Neuroscience
publication_identifier:
  eissn:
  - 1573-6873
  issn:
  - 0929-5313
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multiscale relevance and informative encoding in neuronal spike trains
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 48
year: '2020'
...
---
_id: '7632'
abstract:
- lang: eng
  text: The posterior parietal cortex (PPC) and frontal motor areas comprise a cortical
    network supporting goal-directed behaviour, with functions including sensorimotor
    transformations and decision making. In primates, this network links performed
    and observed actions via mirror neurons, which fire both when individuals perform
    an action and when they observe the same action performed by a conspecific. Mirror
    neurons are believed to be important for social learning, but it is not known
    whether mirror-like neurons occur in similar networks in other social species,
    such as rodents, or if they can be measured in such models using paradigms where
    observers passively view a demonstrator. Therefore, we imaged Ca2+ responses in
    PPC and secondary motor cortex (M2) while mice performed and observed pellet-reaching
    and wheel-running tasks, and found that cell populations in both areas robustly
    encoded several naturalistic behaviours. However, neural responses to the same
    set of observed actions were absent, although we verified that observer mice were
    attentive to performers and that PPC neurons responded reliably to visual cues.
    Statistical modelling also indicated that executed actions outperformed observed
    actions in predicting neural responses. These results raise the possibility that
    sensorimotor action recognition in rodents could take place outside of the parieto-frontal
    circuit, and underscore that detecting socially-driven neural coding depends critically
    on the species and behavioural paradigm used.
article_number: '5559'
article_processing_charge: No
article_type: original
author:
- first_name: Tuce
  full_name: Tombaz, Tuce
  last_name: Tombaz
- first_name: Benjamin A.
  full_name: Dunn, Benjamin A.
  last_name: Dunn
- first_name: Karoline
  full_name: Hovde, Karoline
  last_name: Hovde
- first_name: Ryan J
  full_name: Cubero, Ryan J
  id: 850B2E12-9CD4-11E9-837F-E719E6697425
  last_name: Cubero
  orcid: 0000-0003-0002-1867
- first_name: Bartul
  full_name: Mimica, Bartul
  last_name: Mimica
- first_name: Pranav
  full_name: Mamidanna, Pranav
  last_name: Mamidanna
- first_name: Yasser
  full_name: Roudi, Yasser
  last_name: Roudi
- first_name: Jonathan R.
  full_name: Whitlock, Jonathan R.
  last_name: Whitlock
citation:
  ama: Tombaz T, Dunn BA, Hovde K, et al. Action representation in the mouse parieto-frontal
    network. <i>Scientific reports</i>. 2020;10(1). doi:<a href="https://doi.org/10.1038/s41598-020-62089-6">10.1038/s41598-020-62089-6</a>
  apa: Tombaz, T., Dunn, B. A., Hovde, K., Cubero, R. J., Mimica, B., Mamidanna, P.,
    … Whitlock, J. R. (2020). Action representation in the mouse parieto-frontal network.
    <i>Scientific Reports</i>. Springer Nature. <a href="https://doi.org/10.1038/s41598-020-62089-6">https://doi.org/10.1038/s41598-020-62089-6</a>
  chicago: Tombaz, Tuce, Benjamin A. Dunn, Karoline Hovde, Ryan J Cubero, Bartul Mimica,
    Pranav Mamidanna, Yasser Roudi, and Jonathan R. Whitlock. “Action Representation
    in the Mouse Parieto-Frontal Network.” <i>Scientific Reports</i>. Springer Nature,
    2020. <a href="https://doi.org/10.1038/s41598-020-62089-6">https://doi.org/10.1038/s41598-020-62089-6</a>.
  ieee: T. Tombaz <i>et al.</i>, “Action representation in the mouse parieto-frontal
    network,” <i>Scientific reports</i>, vol. 10, no. 1. Springer Nature, 2020.
  ista: Tombaz T, Dunn BA, Hovde K, Cubero RJ, Mimica B, Mamidanna P, Roudi Y, Whitlock
    JR. 2020. Action representation in the mouse parieto-frontal network. Scientific
    reports. 10(1), 5559.
  mla: Tombaz, Tuce, et al. “Action Representation in the Mouse Parieto-Frontal Network.”
    <i>Scientific Reports</i>, vol. 10, no. 1, 5559, Springer Nature, 2020, doi:<a
    href="https://doi.org/10.1038/s41598-020-62089-6">10.1038/s41598-020-62089-6</a>.
  short: T. Tombaz, B.A. Dunn, K. Hovde, R.J. Cubero, B. Mimica, P. Mamidanna, Y.
    Roudi, J.R. Whitlock, Scientific Reports 10 (2020).
date_created: 2020-04-05T22:00:47Z
date_published: 2020-03-27T00:00:00Z
date_updated: 2023-08-18T10:25:13Z
day: '27'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1038/s41598-020-62089-6
external_id:
  isi:
  - '000560406800007'
file:
- access_level: open_access
  checksum: e6cfaaaf7986532132934400038b824a
  content_type: application/pdf
  creator: dernst
  date_created: 2020-04-06T10:44:23Z
  date_updated: 2020-07-14T12:48:01Z
  file_id: '7644'
  file_name: 2020_ScientificReports_Tombaz.pdf
  file_size: 2621249
  relation: main_file
file_date_updated: 2020-07-14T12:48:01Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
issue: '1'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: Scientific reports
publication_identifier:
  eissn:
  - '20452322'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Action representation in the mouse parieto-frontal network
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2020'
...
---
_id: '7095'
abstract:
- lang: eng
  text: BAX, a member of the BCL2 gene family, controls the committed step of the
    intrinsic apoptotic program. Mitochondrial fragmentation is a commonly observed
    feature of apoptosis, which occurs through the process of mitochondrial fission.
    BAX has consistently been associated with mitochondrial fission, yet how BAX participates
    in the process of mitochondrial fragmentation during apoptosis remains to be tested.
    Time-lapse imaging of BAX recruitment and mitochondrial fragmentation demonstrates
    that rapid mitochondrial fragmentation during apoptosis occurs after the complete
    recruitment of BAX to the mitochondrial outer membrane (MOM). The requirement
    of a fully functioning BAX protein for the fission process was demonstrated further
    in BAX/BAK-deficient HCT116 cells expressing a P168A mutant of BAX. The mutant
    performed fusion to restore the mitochondrial network. but was not demonstrably
    recruited to the MOM after apoptosis induction. Under these conditions, mitochondrial
    fragmentation was blocked. Additionally, we show that loss of the fission protein,
    dynamin-like protein 1 (DRP1), does not temporally affect the initiation time
    or rate of BAX recruitment, but does reduce the final level of BAX recruited to
    the MOM during the late phase of BAX recruitment. These correlative observations
    suggest a model where late-stage BAX oligomers play a functional part of the mitochondrial
    fragmentation machinery in apoptotic cells.
article_number: '16565'
article_processing_charge: No
article_type: original
author:
- first_name: Margaret E
  full_name: Maes, Margaret E
  id: 3838F452-F248-11E8-B48F-1D18A9856A87
  last_name: Maes
  orcid: 0000-0001-9642-1085
- first_name: J. A.
  full_name: Grosser, J. A.
  last_name: Grosser
- first_name: R. L.
  full_name: Fehrman, R. L.
  last_name: Fehrman
- first_name: C. L.
  full_name: Schlamp, C. L.
  last_name: Schlamp
- first_name: R. W.
  full_name: Nickells, R. W.
  last_name: Nickells
citation:
  ama: Maes ME, Grosser JA, Fehrman RL, Schlamp CL, Nickells RW. Completion of BAX
    recruitment correlates with mitochondrial fission during apoptosis. <i>Scientific
    Reports</i>. 2019;9. doi:<a href="https://doi.org/10.1038/s41598-019-53049-w">10.1038/s41598-019-53049-w</a>
  apa: Maes, M. E., Grosser, J. A., Fehrman, R. L., Schlamp, C. L., &#38; Nickells,
    R. W. (2019). Completion of BAX recruitment correlates with mitochondrial fission
    during apoptosis. <i>Scientific Reports</i>. Springer Nature. <a href="https://doi.org/10.1038/s41598-019-53049-w">https://doi.org/10.1038/s41598-019-53049-w</a>
  chicago: Maes, Margaret E, J. A. Grosser, R. L. Fehrman, C. L. Schlamp, and R. W.
    Nickells. “Completion of BAX Recruitment Correlates with Mitochondrial Fission
    during Apoptosis.” <i>Scientific Reports</i>. Springer Nature, 2019. <a href="https://doi.org/10.1038/s41598-019-53049-w">https://doi.org/10.1038/s41598-019-53049-w</a>.
  ieee: M. E. Maes, J. A. Grosser, R. L. Fehrman, C. L. Schlamp, and R. W. Nickells,
    “Completion of BAX recruitment correlates with mitochondrial fission during apoptosis,”
    <i>Scientific Reports</i>, vol. 9. Springer Nature, 2019.
  ista: Maes ME, Grosser JA, Fehrman RL, Schlamp CL, Nickells RW. 2019. Completion
    of BAX recruitment correlates with mitochondrial fission during apoptosis. Scientific
    Reports. 9, 16565.
  mla: Maes, Margaret E., et al. “Completion of BAX Recruitment Correlates with Mitochondrial
    Fission during Apoptosis.” <i>Scientific Reports</i>, vol. 9, 16565, Springer
    Nature, 2019, doi:<a href="https://doi.org/10.1038/s41598-019-53049-w">10.1038/s41598-019-53049-w</a>.
  short: M.E. Maes, J.A. Grosser, R.L. Fehrman, C.L. Schlamp, R.W. Nickells, Scientific
    Reports 9 (2019).
date_created: 2019-11-25T07:45:17Z
date_published: 2019-11-12T00:00:00Z
date_updated: 2023-08-30T07:26:54Z
day: '12'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1038/s41598-019-53049-w
external_id:
  isi:
  - '000495857600019'
  pmid:
  - '31719602'
file:
- access_level: open_access
  checksum: 9ab397ed9c1c454b34bffb8cc863d734
  content_type: application/pdf
  creator: dernst
  date_created: 2019-11-25T07:49:52Z
  date_updated: 2020-07-14T12:47:49Z
  file_id: '7096'
  file_name: 2019_ScientificReports_Maes.pdf
  file_size: 6467393
  relation: main_file
file_date_updated: 2020-07-14T12:47:49Z
has_accepted_license: '1'
intvolume: '         9'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: Scientific Reports
publication_identifier:
  eissn:
  - 2045-2322
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Completion of BAX recruitment correlates with mitochondrial fission during
  apoptosis
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 9
year: '2019'
...
---
_id: '6412'
abstract:
- lang: eng
  text: Polycomb group (PcG) proteins play critical roles in the epigenetic inheritance
    of cell fate. The Polycomb Repressive Complexes PRC1 and PRC2 catalyse distinct
    chromatin modifications to enforce gene silencing, but how transcriptional repression
    is propagated through mitotic cell divisions remains a key unresolved question.
    Using reversible tethering of PcG proteins to ectopic sites in mouse embryonic
    stem cells, here we show that PRC1 can trigger transcriptional repression and
    Polycomb-dependent chromatin modifications. We find that canonical PRC1 (cPRC1),
    but not variant PRC1, maintains gene silencing through cell division upon reversal
    of tethering. Propagation of gene repression is sustained by cis-acting histone
    modifications, PRC2-mediated H3K27me3 and cPRC1-mediated H2AK119ub1, promoting
    a sequence-independent feedback mechanism for PcG protein recruitment. Thus, the
    distinct PRC1 complexes present in vertebrates can differentially regulate epigenetic
    maintenance of gene silencing, potentially enabling dynamic heritable responses
    to complex stimuli. Our findings reveal how PcG repression is potentially inherited
    in vertebrates.
article_number: '1931'
article_processing_charge: No
author:
- first_name: Hagar F.
  full_name: Moussa, Hagar F.
  last_name: Moussa
- first_name: Daniel
  full_name: Bsteh, Daniel
  last_name: Bsteh
- first_name: Ramesh
  full_name: Yelagandula, Ramesh
  last_name: Yelagandula
- first_name: Carina
  full_name: Pribitzer, Carina
  last_name: Pribitzer
- first_name: Karin
  full_name: Stecher, Karin
  last_name: Stecher
- first_name: Katarina
  full_name: Bartalska, Katarina
  id: 4D883232-F248-11E8-B48F-1D18A9856A87
  last_name: Bartalska
- first_name: Luca
  full_name: Michetti, Luca
  last_name: Michetti
- first_name: Jingkui
  full_name: Wang, Jingkui
  last_name: Wang
- first_name: Jorge A.
  full_name: Zepeda-Martinez, Jorge A.
  last_name: Zepeda-Martinez
- first_name: Ulrich
  full_name: Elling, Ulrich
  last_name: Elling
- first_name: Jacob I.
  full_name: Stuckey, Jacob I.
  last_name: Stuckey
- first_name: Lindsey I.
  full_name: James, Lindsey I.
  last_name: James
- first_name: Stephen V.
  full_name: Frye, Stephen V.
  last_name: Frye
- first_name: Oliver
  full_name: Bell, Oliver
  last_name: Bell
citation:
  ama: Moussa HF, Bsteh D, Yelagandula R, et al. Canonical PRC1 controls sequence-independent
    propagation of Polycomb-mediated gene silencing. <i>Nature Communications</i>.
    2019;10(1). doi:<a href="https://doi.org/10.1038/s41467-019-09628-6">10.1038/s41467-019-09628-6</a>
  apa: Moussa, H. F., Bsteh, D., Yelagandula, R., Pribitzer, C., Stecher, K., Bartalska,
    K., … Bell, O. (2019). Canonical PRC1 controls sequence-independent propagation
    of Polycomb-mediated gene silencing. <i>Nature Communications</i>. Springer Nature.
    <a href="https://doi.org/10.1038/s41467-019-09628-6">https://doi.org/10.1038/s41467-019-09628-6</a>
  chicago: Moussa, Hagar F., Daniel Bsteh, Ramesh Yelagandula, Carina Pribitzer, Karin
    Stecher, Katarina Bartalska, Luca Michetti, et al. “Canonical PRC1 Controls Sequence-Independent
    Propagation of Polycomb-Mediated Gene Silencing.” <i>Nature Communications</i>.
    Springer Nature, 2019. <a href="https://doi.org/10.1038/s41467-019-09628-6">https://doi.org/10.1038/s41467-019-09628-6</a>.
  ieee: H. F. Moussa <i>et al.</i>, “Canonical PRC1 controls sequence-independent
    propagation of Polycomb-mediated gene silencing,” <i>Nature Communications</i>,
    vol. 10, no. 1. Springer Nature, 2019.
  ista: Moussa HF, Bsteh D, Yelagandula R, Pribitzer C, Stecher K, Bartalska K, Michetti
    L, Wang J, Zepeda-Martinez JA, Elling U, Stuckey JI, James LI, Frye SV, Bell O.
    2019. Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated
    gene silencing. Nature Communications. 10(1), 1931.
  mla: Moussa, Hagar F., et al. “Canonical PRC1 Controls Sequence-Independent Propagation
    of Polycomb-Mediated Gene Silencing.” <i>Nature Communications</i>, vol. 10, no.
    1, 1931, Springer Nature, 2019, doi:<a href="https://doi.org/10.1038/s41467-019-09628-6">10.1038/s41467-019-09628-6</a>.
  short: H.F. Moussa, D. Bsteh, R. Yelagandula, C. Pribitzer, K. Stecher, K. Bartalska,
    L. Michetti, J. Wang, J.A. Zepeda-Martinez, U. Elling, J.I. Stuckey, L.I. James,
    S.V. Frye, O. Bell, Nature Communications 10 (2019).
date_created: 2019-05-13T07:58:35Z
date_published: 2019-04-29T00:00:00Z
date_updated: 2023-08-25T10:31:56Z
day: '29'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1038/s41467-019-09628-6
external_id:
  isi:
  - '000466118700002'
file:
- access_level: open_access
  checksum: 6550a328335396c856db4cbdda7d2994
  content_type: application/pdf
  creator: dernst
  date_created: 2019-05-14T08:45:51Z
  date_updated: 2020-07-14T12:47:29Z
  file_id: '6448'
  file_name: 2019_NatureComm_Moussa.pdf
  file_size: 1223647
  relation: main_file
file_date_updated: 2020-07-14T12:47:29Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  eissn:
  - '20411723'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated
  gene silencing
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2019'
...
---
_id: '6521'
abstract:
- lang: eng
  text: Microglia have emerged as a critical component of neurodegenerative diseases.
    Genetic manipulation of microglia can elucidate their functional impact in disease.
    In neuroscience, recombinant viruses such as lentiviruses and adeno-associated
    viruses (AAVs) have been successfully used to target various cell types in the
    brain, although effective transduction of microglia is rare. In this review, we
    provide a short background of lentiviruses and AAVs, and strategies for designing
    recombinant viral vectors. Then, we will summarize recent literature on successful
    microglial transductions in vitro and in vivo, and discuss the current challenges.
    Finally, we provide guidelines for reporting the efficiency and specificity of
    viral targeting in microglia, which will enable the microglial research community
    to assess and improve methodologies for future studies.
article_number: '134310'
article_processing_charge: No
article_type: original
author:
- first_name: Margaret E
  full_name: Maes, Margaret E
  id: 3838F452-F248-11E8-B48F-1D18A9856A87
  last_name: Maes
  orcid: 0000-0001-9642-1085
- first_name: Gloria
  full_name: Colombo, Gloria
  id: 3483CF6C-F248-11E8-B48F-1D18A9856A87
  last_name: Colombo
  orcid: 0000-0001-9434-8902
- first_name: Rouven
  full_name: Schulz, Rouven
  id: 4C5E7B96-F248-11E8-B48F-1D18A9856A87
  last_name: Schulz
  orcid: 0000-0001-5297-733X
- first_name: Sandra
  full_name: Siegert, Sandra
  id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
  last_name: Siegert
  orcid: 0000-0001-8635-0877
citation:
  ama: 'Maes ME, Colombo G, Schulz R, Siegert S. Targeting microglia with lentivirus
    and AAV: Recent advances and remaining challenges. <i>Neuroscience Letters</i>.
    2019;707. doi:<a href="https://doi.org/10.1016/j.neulet.2019.134310">10.1016/j.neulet.2019.134310</a>'
  apa: 'Maes, M. E., Colombo, G., Schulz, R., &#38; Siegert, S. (2019). Targeting
    microglia with lentivirus and AAV: Recent advances and remaining challenges. <i>Neuroscience
    Letters</i>. Elsevier. <a href="https://doi.org/10.1016/j.neulet.2019.134310">https://doi.org/10.1016/j.neulet.2019.134310</a>'
  chicago: 'Maes, Margaret E, Gloria Colombo, Rouven Schulz, and Sandra Siegert. “Targeting
    Microglia with Lentivirus and AAV: Recent Advances and Remaining Challenges.”
    <i>Neuroscience Letters</i>. Elsevier, 2019. <a href="https://doi.org/10.1016/j.neulet.2019.134310">https://doi.org/10.1016/j.neulet.2019.134310</a>.'
  ieee: 'M. E. Maes, G. Colombo, R. Schulz, and S. Siegert, “Targeting microglia with
    lentivirus and AAV: Recent advances and remaining challenges,” <i>Neuroscience
    Letters</i>, vol. 707. Elsevier, 2019.'
  ista: 'Maes ME, Colombo G, Schulz R, Siegert S. 2019. Targeting microglia with lentivirus
    and AAV: Recent advances and remaining challenges. Neuroscience Letters. 707,
    134310.'
  mla: 'Maes, Margaret E., et al. “Targeting Microglia with Lentivirus and AAV: Recent
    Advances and Remaining Challenges.” <i>Neuroscience Letters</i>, vol. 707, 134310,
    Elsevier, 2019, doi:<a href="https://doi.org/10.1016/j.neulet.2019.134310">10.1016/j.neulet.2019.134310</a>.'
  short: M.E. Maes, G. Colombo, R. Schulz, S. Siegert, Neuroscience Letters 707 (2019).
date_created: 2019-06-05T13:16:24Z
date_published: 2019-08-10T00:00:00Z
date_updated: 2023-08-28T09:30:57Z
day: '10'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1016/j.neulet.2019.134310
ec_funded: 1
external_id:
  isi:
  - '000486094600037'
  pmid:
  - '31158432'
file:
- access_level: open_access
  checksum: 553c9dbd39727fbed55ee991c51ca4d1
  content_type: application/pdf
  creator: dernst
  date_created: 2019-06-08T11:44:20Z
  date_updated: 2020-07-14T12:47:33Z
  file_id: '6551'
  file_name: 2019_Neuroscience_Maes.pdf
  file_size: 1779287
  relation: main_file
file_date_updated: 2020-07-14T12:47:33Z
has_accepted_license: '1'
intvolume: '       707'
isi: 1
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '665385'
  name: International IST Doctoral Program
- _id: 25D4A630-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '715571'
  name: Microglia action towards neuronal circuit formation and function in health
    and disease
- _id: 267F75D8-B435-11E9-9278-68D0E5697425
  name: Modulating microglia through G protein-coupled receptor (GPCR) signaling
publication: Neuroscience Letters
publication_identifier:
  issn:
  - 0304-3940
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Targeting microglia with lentivirus and AAV: Recent advances and remaining
  challenges'
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 707
year: '2019'
...
---
_id: '32'
abstract:
- lang: eng
  text: The functional role of AMPA receptor (AMPAR)-mediated synaptic signaling between
    neurons and oligodendrocyte precursor cells (OPCs) remains enigmatic. We modified
    the properties of AMPARs at axon-OPC synapses in the mouse corpus callosum in
    vivo during the peak of myelination by targeting the GluA2 subunit. Expression
    of the unedited (Ca2+ permeable) or the pore-dead GluA2 subunit of AMPARs triggered
    proliferation of OPCs and reduced their differentiation into oligodendrocytes.
    Expression of the cytoplasmic C-terminal (GluA2(813-862)) of the GluA2 subunit
    (C-tail), a modification designed to affect the interaction between GluA2 and
    AMPAR-binding proteins and to perturb trafficking of GluA2-containing AMPARs,
    decreased the differentiation of OPCs without affecting their proliferation. These
    findings suggest that ionotropic and non-ionotropic properties of AMPARs in OPCs,
    as well as specific aspects of AMPAR-mediated signaling at axon-OPC synapses in
    the mouse corpus callosum, are important for balancing the response of OPCs to
    proliferation and differentiation cues. In the brain, oligodendrocyte precursor
    cells (OPCs) receive glutamatergic AMPA-receptor-mediated synaptic input from
    neurons. Chen et al. show that modifying AMPA-receptor properties at axon-OPC
    synapses alters proliferation and differentiation of OPCs. This expands the traditional
    view of synaptic transmission by suggesting neurons also use synapses to modulate
    behavior of glia.
acknowledgement: This work was supported by Deutsche Forschungsgemeinschaft (DFG)
  grant KU2569/1-1 (to M.K.); DFG project EXC307Centre for Integrative Neuroscience
  (CIN), including grant Pool Project 2011-12 (jointly to M.K. and I.E.); and the
  Charitable Hertie Foundation (to I.E.). CIN is an Excellence Cluster funded by the
  DFG within the framework of the Excellence Initiative for 2008–2018. M.K. is supported
  by the Tistou & Charlotte Kerstan Foundation.
article_processing_charge: No
author:
- first_name: Ting
  full_name: Chen, Ting
  last_name: Chen
- first_name: Bartosz
  full_name: Kula, Bartosz
  last_name: Kula
- first_name: Balint
  full_name: Nagy, Balint
  id: 30F830CE-02D1-11E9-9BAA-DAF4881429F2
  last_name: Nagy
  orcid: 0000-0002-4002-4686
- first_name: Ruxandra
  full_name: Barzan, Ruxandra
  last_name: Barzan
- first_name: Andrea
  full_name: Gall, Andrea
  last_name: Gall
- first_name: Ingrid
  full_name: Ehrlich, Ingrid
  last_name: Ehrlich
- first_name: Maria
  full_name: Kukley, Maria
  last_name: Kukley
citation:
  ama: Chen T, Kula B, Nagy B, et al. In Vivo regulation of Oligodendrocyte processor
    cell proliferation and differentiation by the AMPA-receptor Subunit GluA2. <i>Cell
    Reports</i>. 2018;25(4):852-861.e7. doi:<a href="https://doi.org/10.1016/j.celrep.2018.09.066">10.1016/j.celrep.2018.09.066</a>
  apa: Chen, T., Kula, B., Nagy, B., Barzan, R., Gall, A., Ehrlich, I., &#38; Kukley,
    M. (2018). In Vivo regulation of Oligodendrocyte processor cell proliferation
    and differentiation by the AMPA-receptor Subunit GluA2. <i>Cell Reports</i>. Elsevier.
    <a href="https://doi.org/10.1016/j.celrep.2018.09.066">https://doi.org/10.1016/j.celrep.2018.09.066</a>
  chicago: Chen, Ting, Bartosz Kula, Balint Nagy, Ruxandra Barzan, Andrea Gall, Ingrid
    Ehrlich, and Maria Kukley. “In Vivo Regulation of Oligodendrocyte Processor Cell
    Proliferation and Differentiation by the AMPA-Receptor Subunit GluA2.” <i>Cell
    Reports</i>. Elsevier, 2018. <a href="https://doi.org/10.1016/j.celrep.2018.09.066">https://doi.org/10.1016/j.celrep.2018.09.066</a>.
  ieee: T. Chen <i>et al.</i>, “In Vivo regulation of Oligodendrocyte processor cell
    proliferation and differentiation by the AMPA-receptor Subunit GluA2,” <i>Cell
    Reports</i>, vol. 25, no. 4. Elsevier, p. 852–861.e7, 2018.
  ista: Chen T, Kula B, Nagy B, Barzan R, Gall A, Ehrlich I, Kukley M. 2018. In Vivo
    regulation of Oligodendrocyte processor cell proliferation and differentiation
    by the AMPA-receptor Subunit GluA2. Cell Reports. 25(4), 852–861.e7.
  mla: Chen, Ting, et al. “In Vivo Regulation of Oligodendrocyte Processor Cell Proliferation
    and Differentiation by the AMPA-Receptor Subunit GluA2.” <i>Cell Reports</i>,
    vol. 25, no. 4, Elsevier, 2018, p. 852–861.e7, doi:<a href="https://doi.org/10.1016/j.celrep.2018.09.066">10.1016/j.celrep.2018.09.066</a>.
  short: T. Chen, B. Kula, B. Nagy, R. Barzan, A. Gall, I. Ehrlich, M. Kukley, Cell
    Reports 25 (2018) 852–861.e7.
date_created: 2018-12-11T11:44:16Z
date_published: 2018-10-23T00:00:00Z
date_updated: 2023-09-11T14:13:32Z
day: '23'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1016/j.celrep.2018.09.066
external_id:
  isi:
  - '000448219500005'
file:
- access_level: open_access
  checksum: d9f74277fd57176e04732707d575cf08
  content_type: application/pdf
  creator: dernst
  date_created: 2018-12-17T12:42:57Z
  date_updated: 2020-07-14T12:46:03Z
  file_id: '5703'
  file_name: 2018_CellReports_Chen.pdf
  file_size: 4461997
  relation: main_file
file_date_updated: 2020-07-14T12:46:03Z
has_accepted_license: '1'
intvolume: '        25'
isi: 1
issue: '4'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '10'
oa: 1
oa_version: Published Version
page: 852 - 861.e7
publication: Cell Reports
publication_status: published
publisher: Elsevier
publist_id: '8023'
quality_controlled: '1'
scopus_import: '1'
status: public
title: In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation
  by the AMPA-receptor Subunit GluA2
tmp:
  image: /images/cc_by_nc_nd.png
  legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
  name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
    (CC BY-NC-ND 4.0)
  short: CC BY-NC-ND (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 25
year: '2018'
...
---
_id: '708'
abstract:
- lang: eng
  text: 'In the developing and adult brain, oligodendrocyte precursor cells (OPCs)
    are influenced by neuronal activity: they are involved in synaptic signaling with
    neurons, and their proliferation and differentiation into myelinating glia can
    be altered by transient changes in neuronal firing. An important question that
    has been unanswered is whether OPCs can discriminate different patterns of neuronal
    activity and respond to them in a distinct way. Here, we demonstrate in brain
    slices that the pattern of neuronal activity determines the functional changes
    triggered at synapses between axons and OPCs. Furthermore, we show that stimulation
    of the corpus callosum at different frequencies in vivo affects proliferation
    and differentiation of OPCs in a dissimilar way. Our findings suggest that neurons
    do not influence OPCs in “all-or-none” fashion but use their firing pattern to
    tune the response and behavior of these nonneuronal cells.'
article_number: e2001993
author:
- first_name: Balint
  full_name: Nagy, Balint
  id: 30F830CE-02D1-11E9-9BAA-DAF4881429F2
  last_name: Nagy
  orcid: 0000-0002-4002-4686
- first_name: Anahit
  full_name: Hovhannisyan, Anahit
  last_name: Hovhannisyan
- first_name: Ruxandra
  full_name: Barzan, Ruxandra
  last_name: Barzan
- first_name: Ting
  full_name: Chen, Ting
  last_name: Chen
- first_name: Maria
  full_name: Kukley, Maria
  last_name: Kukley
citation:
  ama: Nagy B, Hovhannisyan A, Barzan R, Chen T, Kukley M. Different patterns of neuronal
    activity trigger distinct responses of oligodendrocyte precursor cells in the
    corpus callosum. <i>PLoS Biology</i>. 2017;15(8). doi:<a href="https://doi.org/10.1371/journal.pbio.2001993">10.1371/journal.pbio.2001993</a>
  apa: Nagy, B., Hovhannisyan, A., Barzan, R., Chen, T., &#38; Kukley, M. (2017).
    Different patterns of neuronal activity trigger distinct responses of oligodendrocyte
    precursor cells in the corpus callosum. <i>PLoS Biology</i>. Public Library of
    Science. <a href="https://doi.org/10.1371/journal.pbio.2001993">https://doi.org/10.1371/journal.pbio.2001993</a>
  chicago: Nagy, Balint, Anahit Hovhannisyan, Ruxandra Barzan, Ting Chen, and Maria
    Kukley. “Different Patterns of Neuronal Activity Trigger Distinct Responses of
    Oligodendrocyte Precursor Cells in the Corpus Callosum.” <i>PLoS Biology</i>.
    Public Library of Science, 2017. <a href="https://doi.org/10.1371/journal.pbio.2001993">https://doi.org/10.1371/journal.pbio.2001993</a>.
  ieee: B. Nagy, A. Hovhannisyan, R. Barzan, T. Chen, and M. Kukley, “Different patterns
    of neuronal activity trigger distinct responses of oligodendrocyte precursor cells
    in the corpus callosum,” <i>PLoS Biology</i>, vol. 15, no. 8. Public Library of
    Science, 2017.
  ista: Nagy B, Hovhannisyan A, Barzan R, Chen T, Kukley M. 2017. Different patterns
    of neuronal activity trigger distinct responses of oligodendrocyte precursor cells
    in the corpus callosum. PLoS Biology. 15(8), e2001993.
  mla: Nagy, Balint, et al. “Different Patterns of Neuronal Activity Trigger Distinct
    Responses of Oligodendrocyte Precursor Cells in the Corpus Callosum.” <i>PLoS
    Biology</i>, vol. 15, no. 8, e2001993, Public Library of Science, 2017, doi:<a
    href="https://doi.org/10.1371/journal.pbio.2001993">10.1371/journal.pbio.2001993</a>.
  short: B. Nagy, A. Hovhannisyan, R. Barzan, T. Chen, M. Kukley, PLoS Biology 15
    (2017).
date_created: 2018-12-11T11:48:03Z
date_published: 2017-08-22T00:00:00Z
date_updated: 2021-01-12T08:11:45Z
day: '22'
ddc:
- '576'
- '610'
department:
- _id: SaSi
doi: 10.1371/journal.pbio.2001993
file:
- access_level: open_access
  checksum: 0c974f430682dc832ea7b27ab5a93124
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:15:35Z
  date_updated: 2020-07-14T12:47:49Z
  file_id: '5156'
  file_name: IST-2017-889-v1+1_journal.pbio.2001993.pdf
  file_size: 18155365
  relation: main_file
file_date_updated: 2020-07-14T12:47:49Z
has_accepted_license: '1'
intvolume: '        15'
issue: '8'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
publication: PLoS Biology
publication_identifier:
  issn:
  - '15449173'
publication_status: published
publisher: Public Library of Science
publist_id: '6983'
pubrep_id: '889'
quality_controlled: '1'
scopus_import: 1
status: public
title: Different patterns of neuronal activity trigger distinct responses of oligodendrocyte
  precursor cells in the corpus callosum
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2017'
...
---
_id: '557'
abstract:
- lang: eng
  text: PURPOSE. Gene therapy of retinal ganglion cells (RGCs) has promise as a powerful
    therapeutic for the rescue and regeneration of these cells after optic nerve damage.
    However, early after damage, RGCs undergo atrophic changes, including gene silencing.
    It is not known if these changes will deleteriously affect transduction and transgene
    expression, or if the therapeutic protein can influence reactivation of the endogenous
    genome. METHODS. Double-transgenic mice carrying a Rosa26-(LoxP)-tdTomato reporter,
    and a mutant allele for the proapoptotic Bax gene were reared. The Bax mutant
    blocks apoptosis, but RGCs still exhibit nuclear atrophy and gene silencing. At
    times ranging from 1 hour to 4 weeks after optic nerve crush (ONC), eyes received
    an intravitreal injection of AAV2 virus carrying the Cre recombinase. Successful
    transduction was monitored by expression of the tdTomato reporter. Immunostaining
    was used to localize tdTomato expression in select cell types. RESULTS. Successful
    transduction of RGCs was achieved at all time points after ONC using AAV2 expressing
    Cre from the phosphoglycerate kinase (Pgk) promoter, but not the CMV promoter.
    ONC promoted an increase in the transduction of cell types in the inner nuclear
    layer, including Müller cells and rod bipolar neurons. There was minimal evidence
    of transduction of amacrine cells and astrocytes in the inner retina or optic
    nerve. CONCLUSIONS. Damaged RGCs can be transduced and at least some endogenous
    genes can be subsequently activated. Optic nerve damage may change retinal architecture
    to allow greater penetration of an AAV2 virus to transduce several additional
    cell types in the inner nuclear layer.
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  full_name: Nickells, Robert
  last_name: Nickells
- first_name: Heather
  full_name: Schmitt, Heather
  last_name: Schmitt
- first_name: Margaret E
  full_name: Maes, Margaret E
  id: 3838F452-F248-11E8-B48F-1D18A9856A87
  last_name: Maes
  orcid: 0000-0001-9642-1085
- first_name: Cassandra
  full_name: Schlamp, Cassandra
  last_name: Schlamp
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  ama: Nickells R, Schmitt H, Maes ME, Schlamp C. AAV2 mediated transduction of the
    mouse retina after optic nerve injury. <i>Investigative Ophthalmology and Visual
    Science</i>. 2017;58(14):6091-6104. doi:<a href="https://doi.org/10.1167/iovs.17-22634">10.1167/iovs.17-22634</a>
  apa: Nickells, R., Schmitt, H., Maes, M. E., &#38; Schlamp, C. (2017). AAV2 mediated
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    and Visual Science</i>. Association for Research in Vision and Ophthalmology.
    <a href="https://doi.org/10.1167/iovs.17-22634">https://doi.org/10.1167/iovs.17-22634</a>
  chicago: Nickells, Robert, Heather Schmitt, Margaret E Maes, and Cassandra Schlamp.
    “AAV2 Mediated Transduction of the Mouse Retina after Optic Nerve Injury.” <i>Investigative
    Ophthalmology and Visual Science</i>. Association for Research in Vision and Ophthalmology,
    2017. <a href="https://doi.org/10.1167/iovs.17-22634">https://doi.org/10.1167/iovs.17-22634</a>.
  ieee: R. Nickells, H. Schmitt, M. E. Maes, and C. Schlamp, “AAV2 mediated transduction
    of the mouse retina after optic nerve injury,” <i>Investigative Ophthalmology
    and Visual Science</i>, vol. 58, no. 14. Association for Research in Vision and
    Ophthalmology, pp. 6091–6104, 2017.
  ista: Nickells R, Schmitt H, Maes ME, Schlamp C. 2017. AAV2 mediated transduction
    of the mouse retina after optic nerve injury. Investigative Ophthalmology and
    Visual Science. 58(14), 6091–6104.
  mla: Nickells, Robert, et al. “AAV2 Mediated Transduction of the Mouse Retina after
    Optic Nerve Injury.” <i>Investigative Ophthalmology and Visual Science</i>, vol.
    58, no. 14, Association for Research in Vision and Ophthalmology, 2017, pp. 6091–104,
    doi:<a href="https://doi.org/10.1167/iovs.17-22634">10.1167/iovs.17-22634</a>.
  short: R. Nickells, H. Schmitt, M.E. Maes, C. Schlamp, Investigative Ophthalmology
    and Visual Science 58 (2017) 6091–6104.
date_created: 2018-12-11T11:47:10Z
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  text: This article provides an introduction to the role of microRNAs in the nervous
    system and outlines their potential involvement in the pathophysiology of schizophrenia,
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author:
- first_name: Lihuei
  full_name: Tsai, Lihuei
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- first_name: Sandra
  full_name: Siegert, Sandra
  id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
  last_name: Siegert
  orcid: 0000-0001-8635-0877
citation:
  ama: Tsai L, Siegert S. How MicroRNAs Are involved in splitting the mind. <i>JAMA
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  apa: Tsai, L., &#38; Siegert, S. (2016). How MicroRNAs Are involved in splitting
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  chicago: Tsai, Lihuei, and Sandra Siegert. “How MicroRNAs Are Involved in Splitting
    the Mind.” <i>JAMA Psychiatry</i>. American Medical Association, 2016. <a href="https://doi.org/10.1001/jamapsychiatry.2015.3144">https://doi.org/10.1001/jamapsychiatry.2015.3144</a>.
  ieee: L. Tsai and S. Siegert, “How MicroRNAs Are involved in splitting the mind,”
    <i>JAMA Psychiatry</i>, vol. 73, no. 4. American Medical Association, pp. 409–410,
    2016.
  ista: Tsai L, Siegert S. 2016. How MicroRNAs Are involved in splitting the mind.
    JAMA Psychiatry. 73(4), 409–410.
  mla: Tsai, Lihuei, and Sandra Siegert. “How MicroRNAs Are Involved in Splitting
    the Mind.” <i>JAMA Psychiatry</i>, vol. 73, no. 4, American Medical Association,
    2016, pp. 409–10, doi:<a href="https://doi.org/10.1001/jamapsychiatry.2015.3144">10.1001/jamapsychiatry.2015.3144</a>.
  short: L. Tsai, S. Siegert, JAMA Psychiatry 73 (2016) 409–410.
date_created: 2018-12-11T11:50:58Z
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title: How MicroRNAs Are involved in splitting the mind
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...
