---
_id: '2855'
abstract:
- lang: eng
  text: Genomic imprinting leads to preferred expression of either the maternal or
    paternal alleles of a subset of genes. Imprinting is essential for mammalian development,
    and its deregulation causes many diseases. However, the functional relevance of
    imprinting at the cellular level is poorly understood for most imprinted genes.
    We used mosaic analysis with double markers (MADM) in mice to create uniparental
    disomies (UPDs) and to visualize imprinting effects with single-cell resolution.
    Although chromosome 12 UPD did not produce detectable phenotypes, chromosome 7
    UPD caused highly significant paternal growth dominance in the liver and lung,
    but not in the brain or heart. A single gene on chromosome 7, encoding the secreted
    insulin-like growth factor 2 (IGF2), accounts for most of the paternal dominance
    effect. Mosaic analyses implied additional imprinted loci on chromosome 7 acting
    cell autonomously to transmit the IGF2 signal. Our study reveals chromosome- and
    cell-type specificity of genomic imprinting effects.
author:
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
- first_name: Randy
  full_name: Johnson, Randy
  last_name: Johnson
- first_name: Liqun
  full_name: Luo, Liqun
  last_name: Luo
citation:
  ama: Hippenmeyer S, Johnson R, Luo L. Mosaic analysis with double markers reveals
    cell type specific paternal growth dominance. <i>Cell Reports</i>. 2013;3(3):960-967.
    doi:<a href="https://doi.org/10.1016/j.celrep.2013.02.002">10.1016/j.celrep.2013.02.002</a>
  apa: Hippenmeyer, S., Johnson, R., &#38; Luo, L. (2013). Mosaic analysis with double
    markers reveals cell type specific paternal growth dominance. <i>Cell Reports</i>.
    Cell Press. <a href="https://doi.org/10.1016/j.celrep.2013.02.002">https://doi.org/10.1016/j.celrep.2013.02.002</a>
  chicago: Hippenmeyer, Simon, Randy Johnson, and Liqun Luo. “Mosaic Analysis with
    Double Markers Reveals Cell Type Specific Paternal Growth Dominance.” <i>Cell
    Reports</i>. Cell Press, 2013. <a href="https://doi.org/10.1016/j.celrep.2013.02.002">https://doi.org/10.1016/j.celrep.2013.02.002</a>.
  ieee: S. Hippenmeyer, R. Johnson, and L. Luo, “Mosaic analysis with double markers
    reveals cell type specific paternal growth dominance,” <i>Cell Reports</i>, vol.
    3, no. 3. Cell Press, pp. 960–967, 2013.
  ista: Hippenmeyer S, Johnson R, Luo L. 2013. Mosaic analysis with double markers
    reveals cell type specific paternal growth dominance. Cell Reports. 3(3), 960–967.
  mla: Hippenmeyer, Simon, et al. “Mosaic Analysis with Double Markers Reveals Cell
    Type Specific Paternal Growth Dominance.” <i>Cell Reports</i>, vol. 3, no. 3,
    Cell Press, 2013, pp. 960–67, doi:<a href="https://doi.org/10.1016/j.celrep.2013.02.002">10.1016/j.celrep.2013.02.002</a>.
  short: S. Hippenmeyer, R. Johnson, L. Luo, Cell Reports 3 (2013) 960–967.
date_created: 2018-12-11T11:59:57Z
date_published: 2013-03-28T00:00:00Z
date_updated: 2021-01-12T07:00:16Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.celrep.2013.02.002
file:
- access_level: open_access
  checksum: 6e977b918e81384cd571ec5a9d812289
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:17:20Z
  date_updated: 2020-07-14T12:45:51Z
  file_id: '5274'
  file_name: IST-2016-405-v1+1_1-s2.0-S2211124713000612-main.pdf
  file_size: 1907211
  relation: main_file
file_date_updated: 2020-07-14T12:45:51Z
has_accepted_license: '1'
intvolume: '         3'
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 960 - 967
publication: Cell Reports
publication_status: published
publisher: Cell Press
publist_id: '3937'
pubrep_id: '405'
quality_controlled: '1'
scopus_import: 1
status: public
title: Mosaic analysis with double markers reveals cell type specific paternal growth
  dominance
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 3
year: '2013'
...
---
_id: '2264'
abstract:
- lang: eng
  text: Faithful progression through the cell cycle is crucial to the maintenance
    and developmental potential of stem cells. Here, we demonstrate that neural stem
    cells (NSCs) and intermediate neural progenitor cells (NPCs) employ a zinc-finger
    transcription factor specificity protein 2 (Sp2) as a cell cycle regulator in
    two temporally and spatially distinct progenitor domains. Differential conditional
    deletion of Sp2 in early embryonic cerebral cortical progenitors, and perinatal
    olfactory bulb progenitors disrupted transitions through G1, G2 and M phases,
    whereas DNA synthesis appeared intact. Cell-autonomous function of Sp2 was identified
    by deletion of Sp2 using mosaic analysis with double markers, which clearly established
    that conditional Sp2-null NSCs and NPCs are M phase arrested in vivo. Importantly,
    conditional deletion of Sp2 led to a decline in the generation of NPCs and neurons
    in the developing and postnatal brains. Our findings implicate Sp2-dependent mechanisms
    as novel regulators of cell cycle progression, the absence of which disrupts neurogenesis
    in the embryonic and postnatal brain.
article_processing_charge: No
author:
- first_name: Huixuan
  full_name: Liang, Huixuan
  last_name: Liang
- first_name: Guanxi
  full_name: Xiao, Guanxi
  last_name: Xiao
- first_name: Haifeng
  full_name: Yin, Haifeng
  last_name: Yin
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
- first_name: Jonathan
  full_name: Horowitz, Jonathan
  last_name: Horowitz
- first_name: Troy
  full_name: Ghashghaei, Troy
  last_name: Ghashghaei
citation:
  ama: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. Neural development
    is dependent on the function of specificity protein 2 in cell cycle progression.
    <i>Development</i>. 2013;140(3):552-561. doi:<a href="https://doi.org/10.1242/dev.085621">10.1242/dev.085621</a>
  apa: Liang, H., Xiao, G., Yin, H., Hippenmeyer, S., Horowitz, J., &#38; Ghashghaei,
    T. (2013). Neural development is dependent on the function of specificity protein
    2 in cell cycle progression. <i>Development</i>. Company of Biologists. <a href="https://doi.org/10.1242/dev.085621">https://doi.org/10.1242/dev.085621</a>
  chicago: Liang, Huixuan, Guanxi Xiao, Haifeng Yin, Simon Hippenmeyer, Jonathan Horowitz,
    and Troy Ghashghaei. “Neural Development Is Dependent on the Function of Specificity
    Protein 2 in Cell Cycle Progression.” <i>Development</i>. Company of Biologists,
    2013. <a href="https://doi.org/10.1242/dev.085621">https://doi.org/10.1242/dev.085621</a>.
  ieee: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, and T. Ghashghaei,
    “Neural development is dependent on the function of specificity protein 2 in cell
    cycle progression,” <i>Development</i>, vol. 140, no. 3. Company of Biologists,
    pp. 552–561, 2013.
  ista: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. 2013. Neural
    development is dependent on the function of specificity protein 2 in cell cycle
    progression. Development. 140(3), 552–561.
  mla: Liang, Huixuan, et al. “Neural Development Is Dependent on the Function of
    Specificity Protein 2 in Cell Cycle Progression.” <i>Development</i>, vol. 140,
    no. 3, Company of Biologists, 2013, pp. 552–61, doi:<a href="https://doi.org/10.1242/dev.085621">10.1242/dev.085621</a>.
  short: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, T. Ghashghaei, Development
    140 (2013) 552–561.
date_created: 2018-12-11T11:56:39Z
date_published: 2013-02-01T00:00:00Z
date_updated: 2021-01-12T06:56:23Z
day: '01'
department:
- _id: SiHi
doi: 10.1242/dev.085621
external_id:
  pmid:
  - '23293287'
intvolume: '       140'
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561788/
month: '02'
oa: 1
oa_version: Submitted Version
page: 552 - 561
pmid: 1
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '4681'
quality_controlled: '1'
scopus_import: 1
status: public
title: Neural development is dependent on the function of specificity protein 2 in
  cell cycle progression
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 140
year: '2013'
...
---
_id: '2303'
abstract:
- lang: eng
  text: MADM (Mosaic Analysis with Double Markers) technology offers a genetic approach
    in mice to visualize and concomitantly manipulate genetically defined cells at
    clonal level and single cell resolution. MADM employs Cre recombinase/loxP-dependent
    interchromosomal mitotic recombination to reconstitute two split marker genes—green
    GFP and red tdTomato—and can label sparse clones of homozygous mutant cells in
    one color and wild-type cells in the other color in an otherwise unlabeled background.
    At present, major MADM applications include lineage tracing, single cell labeling,
    conditional knockouts in small populations of cells and induction of uniparental
    chromosome disomy to assess effects of genomic imprinting. MADM can be applied
    universally in the mouse with the sole limitation being the specificity of the
    promoter controlling Cre recombinase expression. Here I review recent developments
    and extensions of the MADM technique and give an overview of the major discoveries
    and progresses enabled by the implementation of the novel genetic MADM tools.
acknowledgement: This work was supported by IST Austria institutional funds.
article_type: review
author:
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
citation:
  ama: Hippenmeyer S. Dissection of gene function at clonal level using mosaic analysis
    with double markers. <i>Frontiers in Biology</i>. 2013;8(6):557-568. doi:<a href="https://doi.org/10.1007/s11515-013-1279-6">10.1007/s11515-013-1279-6</a>
  apa: Hippenmeyer, S. (2013). Dissection of gene function at clonal level using mosaic
    analysis with double markers. <i>Frontiers in Biology</i>. Springer. <a href="https://doi.org/10.1007/s11515-013-1279-6">https://doi.org/10.1007/s11515-013-1279-6</a>
  chicago: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using
    Mosaic Analysis with Double Markers.” <i>Frontiers in Biology</i>. Springer, 2013.
    <a href="https://doi.org/10.1007/s11515-013-1279-6">https://doi.org/10.1007/s11515-013-1279-6</a>.
  ieee: S. Hippenmeyer, “Dissection of gene function at clonal level using mosaic
    analysis with double markers,” <i>Frontiers in Biology</i>, vol. 8, no. 6. Springer,
    pp. 557–568, 2013.
  ista: Hippenmeyer S. 2013. Dissection of gene function at clonal level using mosaic
    analysis with double markers. Frontiers in Biology. 8(6), 557–568.
  mla: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using Mosaic
    Analysis with Double Markers.” <i>Frontiers in Biology</i>, vol. 8, no. 6, Springer,
    2013, pp. 557–68, doi:<a href="https://doi.org/10.1007/s11515-013-1279-6">10.1007/s11515-013-1279-6</a>.
  short: S. Hippenmeyer, Frontiers in Biology 8 (2013) 557–568.
date_created: 2018-12-11T11:56:52Z
date_published: 2013-09-03T00:00:00Z
date_updated: 2021-01-12T06:56:39Z
day: '03'
department:
- _id: SiHi
doi: 10.1007/s11515-013-1279-6
intvolume: '         8'
issue: '6'
language:
- iso: eng
month: '09'
oa_version: None
page: 557 - 568
publication: Frontiers in Biology
publication_status: published
publisher: Springer
publist_id: '4624'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dissection of gene function at clonal level using mosaic analysis with double
  markers
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2013'
...
---
_id: '2263'
abstract:
- lang: eng
  text: Nestin-cre transgenic mice have been widely used to direct recombination to
    neural stem cells (NSCs) and intermediate neural progenitor cells (NPCs). Here
    we report that a readily utilized, and the only commercially available, Nestin-cre
    line is insufficient for directing recombination in early embryonic NSCs and NPCs.
    Analysis of recombination efficiency in multiple cre-dependent reporters and a
    genetic mosaic line revealed consistent temporal and spatial patterns of recombination
    in NSCs and NPCs. For comparison we utilized a knock-in Emx1cre line and found
    robust recombination in NSCs and NPCs in ventricular and subventricular zones
    of the cerebral cortices as early as embryonic day 12.5. In addition we found
    that the rate of Nestin-cre driven recombination only reaches sufficiently high
    levels in NSCs and NPCs during late embryonic and early postnatal periods. These
    findings are important when commercially available cre lines are considered for
    directing recombination to embryonic NSCs and NPCs.
author:
- first_name: Huixuan
  full_name: Liang, Huixuan
  last_name: Liang
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
- first_name: H.
  full_name: Ghashghaei, H.
  last_name: Ghashghaei
citation:
  ama: Liang H, Hippenmeyer S, Ghashghaei H. A Nestin-cre transgenic mouse is insufficient
    for recombination in early embryonic neural progenitors. <i>Biology open</i>.
    2012;1(12):1200-1203. doi:<a href="https://doi.org/10.1242/bio.20122287">10.1242/bio.20122287</a>
  apa: Liang, H., Hippenmeyer, S., &#38; Ghashghaei, H. (2012). A Nestin-cre transgenic
    mouse is insufficient for recombination in early embryonic neural progenitors.
    <i>Biology Open</i>. The Company of Biologists. <a href="https://doi.org/10.1242/bio.20122287">https://doi.org/10.1242/bio.20122287</a>
  chicago: Liang, Huixuan, Simon Hippenmeyer, and H. Ghashghaei. “A Nestin-Cre Transgenic
    Mouse Is Insufficient for Recombination in Early Embryonic Neural Progenitors.”
    <i>Biology Open</i>. The Company of Biologists, 2012. <a href="https://doi.org/10.1242/bio.20122287">https://doi.org/10.1242/bio.20122287</a>.
  ieee: H. Liang, S. Hippenmeyer, and H. Ghashghaei, “A Nestin-cre transgenic mouse
    is insufficient for recombination in early embryonic neural progenitors,” <i>Biology
    open</i>, vol. 1, no. 12. The Company of Biologists, pp. 1200–1203, 2012.
  ista: Liang H, Hippenmeyer S, Ghashghaei H. 2012. A Nestin-cre transgenic mouse
    is insufficient for recombination in early embryonic neural progenitors. Biology
    open. 1(12), 1200–1203.
  mla: Liang, Huixuan, et al. “A Nestin-Cre Transgenic Mouse Is Insufficient for Recombination
    in Early Embryonic Neural Progenitors.” <i>Biology Open</i>, vol. 1, no. 12, The
    Company of Biologists, 2012, pp. 1200–03, doi:<a href="https://doi.org/10.1242/bio.20122287">10.1242/bio.20122287</a>.
  short: H. Liang, S. Hippenmeyer, H. Ghashghaei, Biology Open 1 (2012) 1200–1203.
date_created: 2018-12-11T11:56:38Z
date_published: 2012-12-15T00:00:00Z
date_updated: 2021-01-12T06:56:23Z
day: '15'
ddc:
- '576'
department:
- _id: SiHi
doi: 10.1242/bio.20122287
file:
- access_level: open_access
  checksum: 605a1800b81227848c361fd6ba7d22ba
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:13:09Z
  date_updated: 2020-07-14T12:45:35Z
  file_id: '4990'
  file_name: IST-2015-387-v1+1_1200.full.pdf
  file_size: 726695
  relation: main_file
file_date_updated: 2020-07-14T12:45:35Z
has_accepted_license: '1'
intvolume: '         1'
issue: '12'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 1200 - 1203
publication: Biology open
publication_status: published
publisher: The Company of Biologists
publist_id: '4682'
pubrep_id: '387'
quality_controlled: '1'
scopus_import: 1
status: public
title: A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic
  neural progenitors
tmp:
  image: /images/cc_by_nc_sa.png
  legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
  name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
    BY-NC-SA 4.0)
  short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2012'
...
