ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Directional Delta and Notch trafficking in Sara endosomes during asymmetric cell division (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-03-20
    Description: Endocytosis has a crucial role during Notch signalling after the asymmetric division of fly sensory organ precursors (SOPs): directional signalling is mediated by differential endocytosis of the ligand Delta and the Notch effector Sanpodo in one of the SOP daughters, pIIb. Here we show a new mechanism of directional signalling on the basis of the trafficking of Delta and Notch molecules already internalized in the SOP and subsequently targeted to the other daughter cell, pIIa. Internalized Delta and Notch traffic to an endosome marked by the protein Sara. During SOP mitosis, Sara endosomes containing Notch and Delta move to the central spindle and then to pIIa. Subsequently, in pIIa (but not in pIIb) Notch appears cleaved in Sara endosomes in a gamma-secretase- and Delta internalization-dependent manner, indicating that the release of the intracellular Notch tail to activate Notch target genes has occurred. We thus uncover a new mechanism to bias signalling even before asymmetric endocytosis of Sanpodo and Delta takes place in the daughter cells: already during SOP mitosis, asymmetric targeting of Delta and Notch-containing Sara endosomes will increase Notch signalling in pIIa and decrease it in pIIb.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coumailleau, F -- Furthauer, M -- Knoblich, J A -- Gonzalez-Gaitan, M -- England -- Nature. 2009 Apr 23;458(7241):1051-5. doi: 10.1038/nature07854. Epub 2009 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Geneva, 30 Quai Ernest-Ansermet, 1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19295516" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid Precursor Protein Secretases/metabolism ; Animal Structures/cytology/metabolism ; Animals ; Cell Differentiation ; Cell Division ; Cell Lineage ; Drosophila Proteins/*metabolism ; Drosophila melanogaster/anatomy & histology/*cytology/genetics/*metabolism ; Endocytosis ; Endosomes/*metabolism ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins/*metabolism ; Mice ; Microfilament Proteins/metabolism ; Mitosis ; Protein Transport ; Receptors, Notch/*metabolism ; Signal Transduction ; Transforming Growth Factor beta/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Polarized endosome dynamics by spindle asymmetry during asymmetric cell division (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-12-15
    Description: During asymmetric division, fate determinants at the cell cortex segregate unequally into the two daughter cells. It has recently been shown that Sara (Smad anchor for receptor activation) signalling endosomes in the cytoplasm also segregate asymmetrically during asymmetric division. Biased dispatch of Sara endosomes mediates asymmetric Notch/Delta signalling during the asymmetric division of sensory organ precursors in Drosophila. In flies, this has been generalized to stem cells in the gut and the central nervous system, and, in zebrafish, to neural precursors of the spinal cord. However, the mechanism of asymmetric endosome segregation is not understood. Here we show that the plus-end kinesin motor Klp98A targets Sara endosomes to the central spindle, where they move bidirectionally on an antiparallel array of microtubules. The microtubule depolymerizing kinesin Klp10A and its antagonist Patronin generate central spindle asymmetry. This asymmetric spindle, in turn, polarizes endosome motility, ultimately causing asymmetric endosome dispatch into one daughter cell. We demonstrate this mechanism by inverting the polarity of the central spindle by polar targeting of Patronin using nanobodies (single-domain antibodies). This spindle inversion targets the endosomes to the wrong cell. Our data uncover the molecular and physical mechanism by which organelles localized away from the cellular cortex can be dispatched asymmetrically during asymmetric division.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Derivery, Emmanuel -- Seum, Carole -- Daeden, Alicia -- Loubery, Sylvain -- Holtzer, Laurent -- Julicher, Frank -- Gonzalez-Gaitan, Marcos -- England -- Nature. 2015 Dec 10;528(7581):280-5. doi: 10.1038/nature16443.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Faculty of Sciences, University of Geneva, 30 Quai Ernest Ansermet, Geneva 1211, Switzerland. ; Max Planck Institute for the Physics of Complex Systems, Nothnitzer Strasse 38, 01187 Dresden, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26659188" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asymmetric Cell Division/*physiology ; Cell Polarity ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/*cytology/genetics ; Endosomes/*metabolism ; Kinesin/genetics/*metabolism ; Microtubule-Associated Proteins/metabolism ; Sequence Deletion ; Single-Domain Antibodies ; Spindle Apparatus/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...