@article{10815,
  abstract     = {In the last several decades, developmental biology has clarified the molecular mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated that the “tool-kit genes” essential for regulating developmental processes are not only highly conserved among species, but are also used as systems at various times and places in an organism to control distinct developmental events. Therefore, mutations in many of these tool-kit genes may cause congenital diseases involving morphological abnormalities. This link between genes and abnormal morphological phenotypes underscores the importance of understanding how cells behave and contribute to morphogenesis as a result of gene function. Recent improvements in live imaging and in quantitative analyses of cellular dynamics will advance our understanding of the cellular pathogenesis of congenital diseases associated with aberrant morphologies. In these studies, it is critical to select an appropriate model organism for the particular phenomenon of interest.},
  author       = {Hashimoto, Masakazu and Morita, Hitoshi and Ueno, Naoto},
  issn         = {0914-3505},
  journal      = {Congenital Anomalies},
  keywords     = {Developmental Biology, Embryology, General Medicine, Pediatrics, Perinatology, and Child Health},
  number       = {1},
  pages        = {1--7},
  publisher    = {Wiley},
  title        = {{Molecular and cellular mechanisms of development underlying congenital diseases}},
  doi          = {10.1111/cga.12039},
  volume       = {54},
  year         = {2014},
}

@article{11093,
  abstract     = {Nuclear pore complexes (NPCs) are built from ∼30 different proteins called nucleoporins or Nups. Previous studies have shown that several Nups exhibit cell-type-specific expression and that mutations in NPC components result in tissue-specific diseases. Here we show that a specific change in NPC composition is required for both myogenic and neuronal differentiation. The transmembrane nucleoporin Nup210 is absent in proliferating myoblasts and embryonic stem cells (ESCs) but becomes expressed and incorporated into NPCs during cell differentiation. Preventing Nup210 production by RNAi blocks myogenesis and the differentiation of ESCs into neuroprogenitors. We found that the addition of Nup210 to NPCs does not affect nuclear transport but is required for the induction of genes that are essential for cell differentiation. Our results identify a single change in NPC composition as an essential step in cell differentiation and establish a role for Nup210 in gene expression regulation and cell fate determination.},
  author       = {D'Angelo, Maximiliano A. and Gomez-Cavazos, J. Sebastian and Mei, Arianna and Lackner, Daniel H. and HETZER, Martin W},
  issn         = {1534-5807},
  journal      = {Developmental Cell},
  keywords     = {Developmental Biology, Cell Biology, General Biochemistry, Genetics and Molecular Biology, Molecular Biology},
  number       = {2},
  pages        = {446--458},
  publisher    = {Elsevier},
  title        = {{A change in nuclear pore complex composition regulates cell differentiation}},
  doi          = {10.1016/j.devcel.2011.11.021},
  volume       = {22},
  year         = {2012},
}

@article{12199,
  abstract     = {The four microsporangia of the flowering plant anther develop from archesporial cells in the L2 of the primordium. Within each microsporangium, developing microsporocytes are surrounded by concentric monolayers of tapetal, middle layer and endothecial cells. How this intricate array of tissues, each containing relatively few cells, is established in an organ possessing no formal meristems is poorly understood. We describe here the pivotal role of the LRR receptor kinase EXCESS MICROSPOROCYTES 1 (EMS1) in forming the monolayer of tapetal nurse cells in Arabidopsis. Unusually for plants, tapetal cells are specified very early in development, and are subsequently stimulated to proliferate by a receptor-like kinase (RLK) complex that includes EMS1. Mutations in members of this EMS1 signalling complex and its putative ligand result in male-sterile plants in which tapetal initials fail to proliferate. Surprisingly, these cells continue to develop, isolated at the locular periphery. Mutant and wild-type microsporangia expand at similar rates and the ‘tapetal’ space at the periphery of mutant locules becomes occupied by microsporocytes. However, induction of late expression of EMS1 in the few tapetal initials in ems1 plants results in their proliferation to generate a functional tapetum, and this proliferation suppresses microsporocyte number. Our experiments also show that integrity of the tapetal monolayer is crucial for the maintenance of the polarity of divisions within it. This unexpected autonomy of the tapetal ‘lineage’ is discussed in the context of tissue development in complex plant organs, where constancy in size, shape and cell number is crucial.},
  author       = {Feng, Xiaoqi and Dickinson, Hugh G.},
  issn         = {1477-9129},
  journal      = {Development},
  keywords     = {Developmental Biology, Molecular Biology, Anther Tapetum, Arabidopsis, Cell Fate Establishment, EMS1, Reproductive Cell Lineage},
  number       = {14},
  pages        = {2409--2416},
  publisher    = {The Company of Biologists},
  title        = {{Tapetal cell fate, lineage and proliferation in the Arabidopsis anther}},
  doi          = {10.1242/dev.049320},
  volume       = {137},
  year         = {2010},
}

@article{11103,
  abstract     = {Over the last decade, the nuclear envelope (NE) has emerged as a key component in the organization and function of the nuclear genome. As many as 100 different proteins are thought to specifically localize to this double membrane that separates the cytoplasm and the nucleoplasm of eukaryotic cells. Selective portals through the NE are formed at sites where the inner and outer nuclear membranes are fused, and the coincident assembly of ∼30 proteins into nuclear pore complexes occurs. These nuclear pore complexes are essential for the control of nucleocytoplasmic exchange. Many of the NE and nuclear pore proteins are thought to play crucial roles in gene regulation and thus are increasingly linked to human diseases.},
  author       = {HETZER, Martin W and Wente, Susan R.},
  issn         = {1534-5807},
  journal      = {Developmental Cell},
  keywords     = {Developmental Biology, Cell Biology, General Biochemistry, Genetics and Molecular Biology, Molecular Biology},
  number       = {5},
  pages        = {606--616},
  publisher    = {Elsevier},
  title        = {{Border control at the nucleus: Biogenesis and organization of the nuclear membrane and pore complexes}},
  doi          = {10.1016/j.devcel.2009.10.007},
  volume       = {17},
  year         = {2009},
}

@article{11120,
  abstract     = {The nuclear envelope (NE) is a highly specialized membrane that delineates the eukaryotic cell nucleus. It is composed of the inner and outer nuclear membranes, nuclear pore complexes (NPCs) and, in metazoa, the lamina. The NE not only regulates the trafficking of macromolecules between nucleoplasm and cytosol but also provides anchoring sites for chromatin and the cytoskeleton. Through these interactions, the NE helps position the nucleus within the cell and chromosomes within the nucleus, thereby regulating the expression of certain genes. The NE is not static, rather it is continuously remodeled during cell division. The most dramatic example of NE reorganization occurs during mitosis in metazoa when the NE undergoes a complete cycle of disassembly and reformation. Despite the importance of the NE for eukaryotic cell life, relatively little is known about its biogenesis or many of its functions. We thus are far from understanding the molecular etiology of a diverse group of NE-associated diseases.},
  author       = {HETZER, Martin W and Walther, Tobias C. and Mattaj, Iain W.},
  issn         = {1530-8995},
  journal      = {Annual Review of Cell and Developmental Biology},
  keywords     = {Cell Biology, Developmental Biology},
  pages        = {347--380},
  publisher    = {Annual Reviews},
  title        = {{Pushing the envelope: Structure, function, and dynamics of the nuclear periphery}},
  doi          = {10.1146/annurev.cellbio.21.090704.151152},
  volume       = {21},
  year         = {2005},
}

