@article{7399,
  abstract     = {Long non-coding (lnc) RNAs are numerous and found throughout the mammalian genome, and many are thought to be involved in the regulation of gene expression. However, the majority remain relatively uncharacterised and of uncertain function making the use of model systems to uncover their mode of action valuable. Imprinted lncRNAs target and recruit epigenetic silencing factors to a cluster of imprinted genes on the same chromosome, making them one of the best characterized lncRNAs for silencing distant genes in cis. In this study we examined silencing of the distant imprinted gene Slc22a3 by the lncRNA Airn in the Igf2r imprinted cluster in mouse. Previously we proposed that imprinted lncRNAs may silence distant imprinted genes by disrupting promoter-enhancer interactions by being transcribed through the enhancer, which we called the enhancer interference hypothesis. Here we tested this hypothesis by first using allele-specific chromosome conformation capture (3C) to detect interactions between the Slc22a3 promoter and the locus of the Airn lncRNA that silences it on the paternal chromosome. In agreement with the model, we found interactions enriched on the maternal allele across the entire Airn gene consistent with multiple enhancer-promoter interactions. Therefore, to test the enhancer interference hypothesis we devised an approach to delete the entire Airn gene. However, the deletion showed that there are no essential enhancers for Slc22a2, Pde10a and Slc22a3 within the Airn gene, strongly indicating that the Airn RNA rather than its transcription is responsible for silencing distant imprinted genes. Furthermore, we found that silent imprinted genes were covered with large blocks of H3K27me3 on the repressed paternal allele. Therefore we propose an alternative hypothesis whereby the chromosome interactions may initially guide the lncRNA to target imprinted promoters and recruit repressive chromatin, and that these interactions are lost once silencing is established.},
  author       = {Andergassen, Daniel and Muckenhuber, Markus and Bammer, Philipp C. and Kulinski, Tomasz M. and Theussl, Hans-Christian and Shimizu, Takahiko and Penninger, Josef M. and Pauler, Florian and Hudson, Quanah J.},
  issn         = {1553-7404},
  journal      = {PLoS Genetics},
  number       = {7},
  publisher    = {Public Library of Science},
  title        = {{The Airn lncRNA does not require any DNA elements within its locus to silence distant imprinted genes}},
  doi          = {10.1371/journal.pgen.1008268},
  volume       = {15},
  year         = {2019},
}

@article{6830,
  author       = {Contreras, Ximena and Hippenmeyer, Simon},
  issn         = {1097-4199},
  journal      = {Neuron},
  number       = {5},
  pages        = {750--752},
  publisher    = {Elsevier},
  title        = {{Memo1 tiles the radial glial cell grid}},
  doi          = {10.1016/j.neuron.2019.08.021},
  volume       = {103},
  year         = {2019},
}

@article{20,
  abstract     = {Background: Norepinephrine (NE) signaling has a key role in white adipose tissue (WAT) functions, including lipolysis, free fatty acid liberation and, under certain conditions, conversion of white into brite (brown-in-white) adipocytes. However, acute effects of NE stimulation have not been described at the transcriptional network level. Results: We used RNA-seq to uncover a broad transcriptional response. The inference of protein-protein and protein-DNA interaction networks allowed us to identify a set of immediate-early genes (IEGs) with high betweenness, validating our approach and suggesting a hierarchical control of transcriptional regulation. In addition, we identified a transcriptional regulatory network with IEGs as master regulators, including HSF1 and NFIL3 as novel NE-induced IEG candidates. Moreover, a functional enrichment analysis and gene clustering into functional modules suggest a crosstalk between metabolic, signaling, and immune responses. Conclusions: Altogether, our network biology approach explores for the first time the immediate-early systems level response of human adipocytes to acute sympathetic activation, thereby providing a first network basis of early cell fate programs and crosstalks between metabolic and transcriptional networks required for proper WAT function.},
  author       = {Higareda Almaraz, Juan and Karbiener, Michael and Giroud, Maude and Pauler, Florian and Gerhalter, Teresa and Herzig, Stephan and Scheideler, Marcel},
  issn         = {1471-2164},
  journal      = {BMC Genomics},
  number       = {1},
  publisher    = {BioMed Central},
  title        = {{Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes}},
  doi          = {10.1186/s12864-018-5173-0},
  volume       = {19},
  year         = {2018},
}

@misc{9807,
  abstract     = {Table S1. Genes with highest betweenness. Table S2. Local and Master regulators up-regulated. Table S3. Local and Master regulators down-regulated (XLSX 23 kb).},
  author       = {Higareda Almaraz, Juan and Karbiener, Michael and Giroud, Maude and Pauler, Florian and Gerhalter, Teresa and Herzig, Stephan and Scheideler, Marcel},
  publisher    = {Springer Nature},
  title        = {{Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes}},
  doi          = {10.6084/m9.figshare.7295339.v1},
  year         = {2018},
}

@misc{9808,
  abstract     = {Table S4. Counts per Gene per Million Reads Mapped. (XLSX 2751 kb).},
  author       = {Higareda Almaraz, Juan and Karbiener, Michael and Giroud, Maude and Pauler, Florian and Gerhalter, Teresa and Herzig, Stephan and Scheideler, Marcel},
  publisher    = {Springer Nature},
  title        = {{Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes}},
  doi          = {10.6084/m9.figshare.7295369.v1},
  year         = {2018},
}

@unpublished{8547,
  abstract     = {The cerebral cortex contains multiple hierarchically organized areas with distinctive cytoarchitectonical patterns, but the cellular mechanisms underlying the emergence of this diversity remain unclear. Here, we have quantitatively investigated the neuronal output of individual progenitor cells in the ventricular zone of the developing mouse neocortex using a combination of methods that together circumvent the biases and limitations of individual approaches. We found that individual cortical progenitor cells show a high degree of stochasticity and generate pyramidal cell lineages that adopt a wide range of laminar configurations. Mathematical modelling these lineage data suggests that a small number of progenitor cell populations, each generating pyramidal cells following different stochastic developmental programs, suffice to generate the heterogenous complement of pyramidal cell lineages that collectively build the complex cytoarchitecture of the neocortex.},
  author       = {Llorca, Alfredo and Ciceri, Gabriele and Beattie, Robert J and Wong, Fong K. and Diana, Giovanni and Serafeimidou, Eleni and Fernández-Otero, Marian and Streicher, Carmen and Arnold, Sebastian J. and Meyer, Martin and Hippenmeyer, Simon and Maravall, Miguel and Marín, Oscar},
  booktitle    = {bioRxiv},
  title        = {{Heterogeneous progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture}},
  doi          = {10.1101/494088},
  year         = {2018},
}

@article{28,
  abstract     = {This scientific commentary refers to ‘NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice’ by Szczurkowska et al. },
  author       = {Contreras, Ximena and Hippenmeyer, Simon},
  journal      = {Brain a journal of neurology},
  number       = {9},
  pages        = {2542 -- 2544},
  publisher    = {Oxford University Press},
  title        = {{Incorrect trafficking route leads to autism}},
  doi          = {10.1093/brain/awy218},
  volume       = {141},
  year         = {2018},
}

@phdthesis{10,
  abstract     = {Genomic imprinting is an epigenetic process that leads to parent of origin-specific gene expression in a subset of genes. Imprinted genes are essential for brain development, and deregulation of imprinting is associated with neurodevelopmental diseases and the pathogenesis of psychiatric disorders. However, the cell-type specificity of imprinting at single cell resolution, and how imprinting and thus gene dosage regulates neuronal circuit assembly is still largely unknown. Here, MADM (Mosaic Analysis with Double Markers) technology was employed to assess genomic imprinting at single cell level. By visualizing MADM-induced uniparental disomies (UPDs) in distinct colors at single cell level in genetic mosaic animals, this experimental paradigm provides a unique quantitative platform to systematically assay the UPD-mediated imbalances in imprinted gene expression at unprecedented resolution. An experimental pipeline based on FACS, RNA-seq and bioinformatics analysis was established and applied to systematically map cell-type-specific ‘imprintomes’ in the mouse brain. The results revealed that parental-specific expression of imprinted genes per se is rarely cell-type-specific even at the individual cell level. Conversely, when we extended the comparison to downstream responses resulting from imbalanced imprinted gene expression, we discovered an unexpectedly high degree of cell-type specificity. Furthermore, we determined a novel function of genomic imprinting in cortical astrocyte production and in olfactory bulb (OB) granule cell generation. These results suggest important functional implication of genomic imprinting for generating cell-type diversity in the brain. In addition, MADM provides a powerful tool to study candidate genes by concomitant genetic manipulation and fluorescent labelling of single cells. MADM-based candidate gene approach was utilized to identify potential imprinted genes involved in the generation of cortical astrocytes and OB granule cells. We investigated p57Kip2, a maternally expressed gene and known cell cycle regulator. Although we found that p57Kip2 does not play a role in these processes, we detected an unexpected function of the paternal allele previously thought to be silent. Finally, we took advantage of a key property of MADM which is to allow unambiguous investigation of environmental impact on single cells. The experimental pipeline based on FACS and RNA-seq analysis of MADM-labeled cells was established to probe the functional differences of single cell loss of gene function compared to global loss of function on a transcriptional level. With this method, both common and distinct responses were isolated due to cell-autonomous and non-autonomous effects acting on genotypically identical cells. As a result, transcriptional changes were identified which result solely from the surrounding environment. Using the MADM technology to study genomic imprinting at single cell resolution, we have identified cell-type-specific gene expression, novel gene function and the impact of environment on single cell transcriptomes. Together, these provide important insights to the understanding of mechanisms regulating cell-type specificity and thus diversity in the brain.},
  author       = {Laukoter, Susanne},
  issn         = {2663-337X},
  pages        = {1 -- 139},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Role of genomic imprinting in cerebral cortex development}},
  doi          = {10.15479/AT:ISTA:th1057},
  year         = {2018},
}

@article{621,
  abstract     = {The mammalian cerebral cortex is responsible for higher cognitive functions such as perception, consciousness, and acquiring and processing information. The neocortex is organized into six distinct laminae, each composed of a rich diversity of cell types which assemble into highly complex cortical circuits. Radial glia progenitors (RGPs) are responsible for producing all neocortical neurons and certain glia lineages. Here, we discuss recent discoveries emerging from clonal lineage analysis at the single RGP cell level that provide us with an inaugural quantitative framework of RGP lineage progression. We further discuss the importance of the relative contribution of intrinsic gene functions and non-cell-autonomous or community effects in regulating RGP proliferation behavior and lineage progression.},
  author       = {Beattie, Robert J and Hippenmeyer, Simon},
  issn         = {0014-5793},
  journal      = {FEBS letters},
  number       = {24},
  pages        = {3993  -- 4008},
  publisher    = {Wiley-Blackwell},
  title        = {{Mechanisms of radial glia progenitor cell lineage progression}},
  doi          = {10.1002/1873-3468.12906},
  volume       = {591},
  year         = {2017},
}

@article{1016,
  abstract     = {The integrity and dynamic properties of the microtubule cytoskeleton are indispensable for the development of the mammalian brain. Consequently, mutations in the genes that encode the structural component (the α/β-tubulin heterodimer) can give rise to severe, sporadic neurodevelopmental disorders. These are commonly referred to as the tubulinopathies. Here we report the addition of recessive quadrupedalism, also known as Uner Tan syndrome (UTS), to the growing list of diseases caused by tubulin variants. Analysis of a consanguineous UTS family identified a biallelic TUBB2B mutation, resulting in a p.R390Q amino acid substitution. In addition to the identifying quadrupedal locomotion, all three patients showed severe cerebellar hypoplasia. None, however, displayed the basal ganglia malformations typically associated with TUBB2B mutations. Functional analysis of the R390Q substitution revealed that it did not affect the ability of β-tubulin to fold or become assembled into the α/β-heterodimer, nor did it influence the incorporation of mutant-containing heterodimers into microtubule polymers. The 390Q mutation in S. cerevisiae TUB2 did not affect growth under basal conditions, but did result in increased sensitivity to microtubule-depolymerizing drugs, indicative of a mild impact of this mutation on microtubule function. The TUBB2B mutation described here represents an unusual recessive mode of inheritance for missense-mediated tubulinopathies and reinforces the sensitivity of the developing cerebellum to microtubule defects.},
  author       = {Breuss, Martin and Nguyen, Thai and Srivatsan, Anjana and Leca, Ines and Tian, Guoling and Fritz, Tanja and Hansen, Andi H and Musaev, Damir and Mcevoy Venneri, Jennifer and Kiely, James and Rosti, Rasim and Scott, Eric and Tan, Uner and Kolodner, Richard and Cowan, Nicholas and Keays, David and Gleeson, Joseph},
  issn         = {0964-6906},
  journal      = {Human Molecular Genetics},
  number       = {2},
  pages        = {258 -- 269},
  publisher    = {Oxford University Press},
  title        = {{Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability}},
  doi          = {10.1093/hmg/ddw383},
  volume       = {26},
  year         = {2017},
}

@article{1017,
  abstract     = {The development of the vertebrate central nervous system is reliant on a complex cascade of biological processes that include mitotic division, relocation of migrating neurons, and the extension of dendritic and axonal processes. Each of these cellular events requires the diverse functional repertoire of the microtubule cytoskeleton for the generation of forces, assembly of macromolecular complexes and transport of molecules and organelles. The tubulins are a multi-gene family that encode for the constituents of microtubules, and have been implicated in a spectrum of neurological disorders. Evidence is building that different tubulins tune the functional properties of the microtubule cytoskeleton dependent on the cell type, developmental profile and subcellular localisation. Here we review of the origins of the functional specification of the tubulin gene family in the developing brain at a transcriptional, translational, and post-transcriptional level. We remind the reader that tubulins are not just loading controls for your average Western blot.},
  author       = {Breuss, Martin and Leca, Ines and Gstrein, Thomas and Hansen, Andi H and Keays, David},
  issn         = {1044-7431},
  journal      = {Molecular and Cellular Neuroscience},
  pages        = {58 -- 67},
  publisher    = {Academic Press},
  title        = {{Tubulins and brain development: The origins of functional specification}},
  doi          = {10.1016/j.mcn.2017.03.002},
  volume       = {84},
  year         = {2017},
}

@article{805,
  abstract     = {During corticogenesis, distinct classes of neurons are born from progenitor cells located in the ventricular and subventricular zones, from where they migrate towards the pial surface to assemble into highly organized layer-specific circuits. However, the precise and coordinated transcriptional network activity defining neuronal identity is still not understood. Here, we show that genetic depletion of the basic helix-loop-helix (bHLH) transcription factor E2A splice variant E47 increased the number of Tbr1-positive deep layer and Satb2-positive upper layer neurons at E14.5, while depletion of the alternatively spliced E12 variant did not affect layer-specific neurogenesis. While ChIP-Seq identified a big overlap for E12- and E47-specific binding sites in embryonic NSCs, including sites at the cyclin-dependent kinase inhibitor (CDKI) Cdkn1c gene locus, RNA-Seq revealed a unique transcriptional regulation by each splice variant. E47 activated the expression of the CDKI Cdkn1c through binding to a distal enhancer. Finally, overexpression of E47 in embryonic NSCs in vitro impaired neurite outgrowth and E47 overexpression in vivo by in utero electroporation disturbed proper layer-specific neurogenesis and upregulated p57(KIP2) expression. Overall, this study identified E2A target genes in embryonic NSCs and demonstrates that E47 regulates neuronal differentiation via p57(KIP2).},
  author       = {Pfurr, Sabrina and Chu, Yu and Bohrer, Christian and Greulich, Franziska and Beattie, Robert J and Mammadzada, Könül and Hils, Miriam and Arnold, Sebastian and Taylor, Verdon and Schachtrup, Kristina and Uhlenhaut, N Henriette and Schachtrup, Christian},
  journal      = {Development},
  pages        = {3917 -- 3931},
  publisher    = {Company of Biologists},
  title        = {{The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development}},
  doi          = {10.1242/dev.145698},
  volume       = {144},
  year         = {2017},
}

@article{944,
  abstract     = {The concerted production of neurons and glia by neural stem cells (NSCs) is essential for neural circuit assembly. In the developing cerebral cortex, radial glia progenitors (RGPs) generate nearly all neocortical neurons and certain glia lineages. RGP proliferation behavior shows a high degree of non-stochasticity, thus a deterministic characteristic of neuron and glia production. However, the cellular and molecular mechanisms controlling RGP behavior and proliferation dynamics in neurogenesis and glia generation remain unknown. By using mosaic analysis with double markers (MADM)-based genetic paradigms enabling the sparse and global knockout with unprecedented single-cell resolution, we identified Lgl1 as a critical regulatory component. We uncover Lgl1-dependent tissue-wide community effects required for embryonic cortical neurogenesis and novel cell-autonomous Lgl1 functions controlling RGP-mediated glia genesis and postnatal NSC behavior. These results suggest that NSC-mediated neuron and glia production is tightly regulated through the concerted interplay of sequential Lgl1-dependent global and cell intrinsic mechanisms.},
  author       = {Beattie, Robert J and Postiglione, Maria P and Burnett, Laura and Laukoter, Susanne and Streicher, Carmen and Pauler, Florian and Xiao, Guanxi and Klezovitch, Olga and Vasioukhin, Valeri and Ghashghaei, Troy and Hippenmeyer, Simon},
  issn         = {0896-6273},
  journal      = {Neuron},
  number       = {3},
  pages        = {517 -- 533.e3},
  publisher    = {Cell Press},
  title        = {{Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells}},
  doi          = {10.1016/j.neuron.2017.04.012},
  volume       = {94},
  year         = {2017},
}

@misc{9707,
  abstract     = {Branching morphogenesis of the epithelial ureteric bud forms the renal collecting duct system and is critical for normal nephron number, while low nephron number is implicated in hypertension and renal disease. Ureteric bud growth and branching requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling up-regulates transcription factors Etv4 and Etv5, which are also critical for branching. Despite extensive knowledge of the genetic control of these events, it is not understood, at the cellular level, how renal branching morphogenesis is achieved or how Ret signaling influences epithelial cell behaviors to promote this process. Analysis of chimeric embryos previously suggested a role for Ret signaling in promoting cell rearrangements in the nephric duct, but this method was unsuited to study individual cell behaviors during ureteric bud branching. Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture and time-lapse imaging, to trace the movements and divisions of individual ureteric bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type clones in which the mutant and wild-type sister cells are differentially and heritably marked by green and red fluorescent proteins. We find that, in normal kidneys, most individual tip cells behave as self-renewing progenitors, some of whose progeny remain at the tips while others populate the growing UB trunks. In Ret or Etv4 MADM clones, the wild-type cells generated at a UB tip are much more likely to remain at, or move to, the new tips during branching and elongation, while their Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks. By tracking successive mitoses in a cell lineage, we find that Ret signaling has little effect on proliferation, in contrast to its effects on cell movement. Our results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric bud tips, and suggest a model in which these cell movements mediate branching morphogenesis.},
  author       = {Riccio, Paul and Cebrián, Christina and Zong, Hui and Hippenmeyer, Simon and Costantini, Frank},
  publisher    = {Dryad},
  title        = {{Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis}},
  doi          = {10.5061/dryad.pk16b},
  year         = {2017},
}

@article{713,
  abstract     = {To determine the dynamics of allelic-specific expression during mouse development, we analyzed RNA-seq data from 23 F1 tissues from different developmental stages, including 19 female tissues allowing X chromosome inactivation (XCI) escapers to also be detected. We demonstrate that allelic expression arising from genetic or epigenetic differences is highly tissue-specific. We find that tissue-specific strain-biased gene expression may be regulated by tissue-specific enhancers or by post-transcriptional differences in stability between the alleles. We also find that escape from X-inactivation is tissue-specific, with leg muscle showing an unexpectedly high rate of XCI escapers. By surveying a range of tissues during development, and performing extensive validation, we are able to provide a high confidence list of mouse imprinted genes including 18 novel genes. This shows that cluster size varies dynamically during development and can be substantially larger than previously thought, with the Igf2r cluster extending over 10 Mb in placenta.},
  author       = {Andergassen, Daniel and Dotter, Christoph and Wenzel, Dyniel and Sigl, Verena and Bammer, Philipp and Muckenhuber, Markus and Mayer, Daniela and Kulinski, Tomasz and Theussl, Hans and Penninger, Josef and Bock, Christoph and Barlow, Denise and Pauler, Florian and Hudson, Quanah},
  issn         = {2050-084X},
  journal      = {eLife},
  publisher    = {eLife Sciences Publications},
  title        = {{Mapping the mouse Allelome reveals tissue specific regulation of allelic expression}},
  doi          = {10.7554/eLife.25125},
  volume       = {6},
  year         = {2017},
}

@article{960,
  abstract     = {The human cerebral cortex is the seat of our cognitive abilities and composed of an extraordinary number of neurons, organized in six distinct layers. The establishment of specific morphological and physiological features in individual neurons needs to be regulated with high precision. Impairments in the sequential developmental programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture which is thought to represent the major underlying cause for several neurological disorders including neurodevelopmental and psychiatric diseases. In this review we discuss the role of cell polarity at sequential stages during cortex development. We first provide an overview of morphological cell polarity features in cortical neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual molecular and biochemical framework how cell polarity is established at the cellular level through a break in symmetry in nascent cortical projection neurons. Lastly we provide a perspective how the molecular mechanisms applying to single cells could be probed and integrated in an in vivo and tissue-wide context.},
  author       = {Hansen, Andi H and Düllberg, Christian F and Mieck, Christine and Loose, Martin and Hippenmeyer, Simon},
  issn         = {1662-5102},
  journal      = {Frontiers in Cellular Neuroscience},
  publisher    = {Frontiers Research Foundation},
  title        = {{Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks}},
  doi          = {10.3389/fncel.2017.00176},
  volume       = {11},
  year         = {2017},
}

@article{1181,
  abstract     = {This review accompanies a 2016 SFN mini-symposium presenting examples of current studies that address a central question: How do neural stem cells (NSCs) divide in different ways to produce heterogeneous daughter types at the right time and in proper numbers to build a cerebral cortex with the appropriate size and structure? We will focus on four aspects of corticogenesis: cytokinesis events that follow apical mitoses of NSCs; coordinating abscission with delamination from the apical membrane; timing of neurogenesis and its indirect regulation through emergence of intermediate progenitors; and capacity of single NSCs to generate the correct number and laminar fate of cortical neurons. Defects in these mechanisms can cause microcephaly and other brain malformations, and understanding them is critical to designing diagnostic tools and preventive and corrective therapies.},
  author       = {Dwyer, Noelle and Chen, Bin and Chou, Shen and Hippenmeyer, Simon and Nguyen, Laurent and Ghashghaei, Troy},
  journal      = {Journal of Neuroscience},
  number       = {45},
  pages        = {11394 -- 11401},
  publisher    = {Society for Neuroscience},
  title        = {{Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity}},
  doi          = {10.1523/JNEUROSCI.2359-16.2016},
  volume       = {36},
  year         = {2016},
}

@article{1488,
  abstract     = {Branching morphogenesis of the epithelial ureteric bud forms the renal collecting duct system and is critical for normal nephron number, while low nephron number is implicated in hypertension and renal disease. Ureteric bud growth and branching requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling up-regulates transcription factors Etv4 and Etv5, which are also critical for branching. Despite extensive knowledge of the genetic control of these events, it is not understood, at the cellular level, how renal branching morphogenesis is achieved or how Ret signaling influences epithelial cell behaviors to promote this process. Analysis of chimeric embryos previously suggested a role for Ret signaling in promoting cell rearrangements in the nephric duct, but this method was unsuited to study individual cell behaviors during ureteric bud branching. Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture and time-lapse imaging, to trace the movements and divisions of individual ureteric bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type clones in which the mutant and wild-type sister cells are differentially and heritably marked by green and red fluorescent proteins. We find that, in normal kidneys, most individual tip cells behave as self-renewing progenitors, some of whose progeny remain at the tips while others populate the growing UB trunks. In Ret or Etv4 MADM clones, the wild-type cells generated at a UB tip are much more likely to remain at, or move to, the new tips during branching and elongation, while their Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks. By tracking successive mitoses in a cell lineage, we find that Ret signaling has little effect on proliferation, in contrast to its effects on cell movement. Our results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric bud tips, and suggest a model in which these cell movements mediate branching morphogenesis.},
  author       = {Riccio, Paul and Cebrián, Cristina and Zong, Hui and Hippenmeyer, Simon and Costantini, Frank},
  journal      = {PLoS Biology},
  number       = {2},
  publisher    = {Public Library of Science},
  title        = {{Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis}},
  doi          = {10.1371/journal.pbio.1002382},
  volume       = {14},
  year         = {2016},
}

@article{1550,
  abstract     = {The medial ganglionic eminence (MGE) gives rise to the majority of mouse forebrain interneurons. Here, we examine the lineage relationship among MGE-derived interneurons using a replication-defective retroviral library containing a highly diverse set of DNA barcodes. Recovering the barcodes from the mature progeny of infected progenitor cells enabled us to unambiguously determine their respective lineal relationship. We found that clonal dispersion occurs across large areas of the brain and is not restricted by anatomical divisions. As such, sibling interneurons can populate the cortex, hippocampus striatum, and globus pallidus. The majority of interneurons appeared to be generated from asymmetric divisions of MGE progenitor cells, followed by symmetric divisions within the subventricular zone. Altogether, our findings uncover that lineage relationships do not appear to determine interneuron allocation to particular regions. As such, it is likely that clonally related interneurons have considerable flexibility as to the particular forebrain circuits to which they can contribute.},
  author       = {Mayer, Christian and Jaglin, Xavier and Cobbs, Lucy and Bandler, Rachel and Streicher, Carmen and Cepko, Constance and Hippenmeyer, Simon and Fishell, Gord},
  journal      = {Neuron},
  number       = {5},
  pages        = {989 -- 998},
  publisher    = {Elsevier},
  title        = {{Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries}},
  doi          = {10.1016/j.neuron.2015.07.011},
  volume       = {87},
  year         = {2015},
}

@article{2261,
  abstract     = {To reveal the full potential of human pluripotent stem cells, new methods for rapid, site-specific genomic engineering are needed. Here, we describe a system for precise genetic modification of human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). We identified a novel human locus, H11, located in a safe, intergenic, transcriptionally active region of chromosome 22, as the recipient site, to provide robust, ubiquitous expression of inserted genes. Recipient cell lines were established by site-specific placement of a ‘landing pad’ cassette carrying attP sites for phiC31 and Bxb1 integrases at the H11 locus by spontaneous or TALEN-assisted homologous recombination. Dual integrase cassette exchange (DICE) mediated by phiC31 and Bxb1 integrases was used to insert genes of interest flanked by phiC31 and Bxb1 attB sites at the H11 locus, replacing the landing pad. This system provided complete control over content, direction and copy number of inserted genes, with a specificity of 100%. A series of genes, including mCherry and various combinations of the neural transcription factors LMX1a, FOXA2 and OTX2, were inserted in recipient cell lines derived from H9 ESC, as well as iPSC lines derived from a Parkinson’s disease patient and a normal sibling control. The DICE system offers rapid, efficient and precise gene insertion in ESC and iPSC and is particularly well suited for repeated modifications of the same locus.},
  author       = {Zhu, Fangfang and Gamboa, Matthew and Farruggio, Alfonso and Hippenmeyer, Simon and Tasic, Bosiljka and Schüle, Birgitt and Chen Tsai, Yanru and Calos, Michele},
  journal      = {Nucleic Acids Research},
  number       = {5},
  publisher    = {Oxford University Press},
  title        = {{DICE, an efficient system for iterative genomic editing in human pluripotent stem cells}},
  doi          = {10.1093/nar/gkt1290},
  volume       = {42},
  year         = {2014},
}