@article{2303,
  abstract     = {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.},
  author       = {Hippenmeyer, Simon},
  journal      = {Frontiers in Biology},
  number       = {6},
  pages        = {557 -- 568},
  publisher    = {Springer},
  title        = {{Dissection of gene function at clonal level using mosaic analysis with double markers}},
  doi          = {10.1007/s11515-013-1279-6},
  volume       = {8},
  year         = {2013},
}

@article{2838,
  abstract     = {Individuals with Down syndrome (DS) present important motor deficits that derive from altered motor development of infants and young children. DYRK1A, a candidate gene for DS abnormalities has been implicated in motor function due to its expression in motor nuclei in the adult brain, and its overexpression in DS mouse models leads to hyperactivity and altered motor learning. However, its precise role in the adult motor system, or its possible involvement in postnatal locomotor development has not yet been clarified. During the postnatal period we observed time-specific expression of Dyrk1A in discrete subsets of brainstem nuclei and spinal cord motor neurons. Interestingly, we describe for the first time the presence of Dyrk1A in the presynaptic terminal of the neuromuscular junctions and its axonal transport from the facial nucleus, suggesting a function for Dyrk1A in these structures. Relevant to DS, Dyrk1A overexpression in transgenic mice (TgDyrk1A) produces motor developmental alterations possibly contributing to DS motor phenotypes and modifies the numbers of motor cholinergic neurons, suggesting that the kinase may have a role in the development of the brainstem and spinal cord motor system.},
  author       = {Arquè Fuste, Gloria and Casanovas, Anna and Dierssen, Mara},
  journal      = {PLoS One},
  number       = {1},
  publisher    = {Public Library of Science},
  title        = {{Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome}},
  doi          = {10.1371/journal.pone.0054285},
  volume       = {8},
  year         = {2013},
}

@article{2855,
  abstract     = {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       = {Hippenmeyer, Simon and Johnson, Randy and Luo, Liqun},
  journal      = {Cell Reports},
  number       = {3},
  pages        = {960 -- 967},
  publisher    = {Cell Press},
  title        = {{Mosaic analysis with double markers reveals cell type specific paternal growth dominance}},
  doi          = {10.1016/j.celrep.2013.02.002},
  volume       = {3},
  year         = {2013},
}

@article{2263,
  abstract     = {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       = {Liang, Huixuan and Hippenmeyer, Simon and Ghashghaei, H.},
  journal      = {Biology open},
  number       = {12},
  pages        = {1200 -- 1203},
  publisher    = {The Company of Biologists},
  title        = {{A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors}},
  doi          = {10.1242/bio.20122287},
  volume       = {1},
  year         = {2012},
}