@unpublished{21963,
  abstract     = {The cerebral cortex consists of immense numbers of neuronal and glial cell-types derived from radial glial progenitor (RGP) cells. How RGPs generate appropriate quantities of distinct cortical cell-types to safeguard a brain of correct size, is not well understood. However, genetic aberration in human, including mutations in PTEN, lead to cortical malformation such as macrocephaly, albeit with unknown etiology. Here we utilized Mosaic Analysis with Double Markers (MADM)-based clonal analysis and single cell phenotyping to decipher the role of Pten in neurogenic and gliogenic RGP lineage progression during cortical ontogeny. While neurogenic RGP lineage progression and projection neuron production was moderately altered in the absence of Pten, cortical astrocyte production was drastically increased. Through genetic epistasis experiments we show that the loss of Pten uncouples astrocyte generation from essential growth factor signaling hubs, funneling into MAPK. Collectively, our results suggest that Pten regulates RGP lineage progression with distinct sequential functions in cortical projection neurogenesis and astrocyte production to ensure the emergence of a correctly-sized cerebral cortex.},
  author       = {Miranda, Osvaldo and Contreras, Ximena and Pauler, Florian and Davaatseren, Amarbayasgalan and Amberg, Nicole and Streicher, Carmen and Villalba Requena, Ana and Heger, Anna-Magdalena and Marie, Corentine and Hassan, Bassem A. and Rülicke, Thomas and Hippenmeyer, Simon},
  booktitle    = {bioRxiv},
  title        = {{Pten orchestrates neurogenic radial glia lineage progression and tunes neocortical astrocyte production}},
  doi          = {10.64898/2026.05.01.722191},
  year         = {2026},
}

@article{9603,
  abstract     = {Mosaic analysis with double markers (MADM) offers one approach to visualize and concomitantly manipulate genetically defined cells in mice with single-cell resolution. MADM applications include the analysis of lineage, single-cell morphology and physiology, genomic imprinting phenotypes, and dissection of cell-autonomous gene functions in vivo in health and disease. Yet, MADM can only be applied to <25% of all mouse genes on select chromosomes to date. To overcome this limitation, we generate transgenic mice with knocked-in MADM cassettes near the centromeres of all 19 autosomes and validate their use across organs. With this resource, >96% of the entire mouse genome can now be subjected to single-cell genetic mosaic analysis. Beyond a proof of principle, we apply our MADM library to systematically trace sister chromatid segregation in distinct mitotic cell lineages. We find striking chromosome-specific biases in segregation patterns, reflecting a putative mechanism for the asymmetric segregation of genetic determinants in somatic stem cell division.},
  author       = {Contreras, Ximena and Amberg, Nicole and Davaatseren, Amarbayasgalan and Hansen, Andi H and Sonntag, Johanna and Andersen, Lill and Bernthaler, Tina and Streicher, Carmen and Heger, Anna-Magdalena and Johnson, Randy L. and Schwarz, Lindsay A. and Luo, Liqun and Rülicke, Thomas and Hippenmeyer, Simon},
  issn         = {2211-1247},
  journal      = {Cell Reports},
  number       = {12},
  publisher    = {Cell Press},
  title        = {{A genome-wide library of MADM mice for single-cell genetic mosaic analysis}},
  doi          = {10.1016/j.celrep.2021.109274},
  volume       = {35},
  year         = {2021},
}