1. Developmental Biology
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Bicoid gradient formation and function in the Drosophila pre-syncytial blastoderm

  1. Zehra Ali-Murthy
  2. Thomas B Kornberg  Is a corresponding author
  1. University of California, San Francisco, United States
Research Article
  • Cited 15
  • Views 6,384
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Cite this article as: eLife 2016;5:e13222 doi: 10.7554/eLife.13222

Abstract

Bicoid (Bcd) protein distributes in a concentration gradient that organizes the anterior/posterior axis of the Drosophila embryo. It has been understood that bcd RNA is sequestered at the anterior pole during oogenesis, is not translated until fertilization, and produces a protein gradient that functions in the syncytial blastoderm after 9-10 nuclear divisions. However, technical issues limited the sensitivity of analysis of pre-syncytial blastoderm embryos and precluded studies of oocytes after stage 13. We developed methods to analyze stage 14 oocytes and pre-syncytial blastoderm embryos, and found that stage 14 oocytes make Bcd protein, that bcd RNA and Bcd protein distribute in matching concentration gradients in the interior of nuclear cycle 2-6 embryos, and that Bcd regulation of target gene expression is apparent at nuclear cycle 7, two cycles prior to syncytial blastoderm. We discuss the implications for the generation and function of the Bcd gradient.

Article and author information

Author details

  1. Zehra Ali-Murthy

    Cardiovascular Research Institute, University of California, San Francisco, San Francisco, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Thomas B Kornberg

    Cardiovascular Research Institute, University of California, San Francisco, San Francisco, United States
    For correspondence
    tkornberg@ucsf.edu
    Competing interests
    The authors declare that no competing interests exist.

Reviewing Editor

  1. Allan C Spradling, Howard Hughes Medical Institute, Carnegie Institution for Science, United States

Publication history

  1. Received: November 20, 2015
  2. Accepted: February 1, 2016
  3. Accepted Manuscript published: February 17, 2016 (version 1)
  4. Version of Record published: March 1, 2016 (version 2)
  5. Version of Record updated: March 15, 2017 (version 3)

Copyright

© 2016, Ali-Murthy & Kornberg

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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Further reading

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    Mechanical stress during cell migration may be a previously unappreciated source of genome instability, but the extent to which this happens in any animal in vivo remains unknown. We consider an in vivo system where the adult stem cells of planarian flatworms are required to migrate to a distal wound site. We observe a relationship between adult stem cell migration and ongoing DNA damage and repair during tissue regeneration. Migrating planarian stem cells undergo changes in nuclear shape and exhibit increased levels of DNA damage. Increased DNA damage levels reduce once stem cells reach the wound site. Stem cells in which DNA damage is induced prior to wounding take longer to initiate migration and migrating stem cell populations are more sensitive to further DNA damage than stationary stem cells. RNAi-mediated knockdown of DNA repair pathway components blocks normal stem cell migration, confirming that active DNA repair pathways are required to allow successful migration to a distal wound site. Together these findings provide evidence that levels of migration-coupled-DNA-damage are significant in adult stem cells and that ongoing migration requires DNA repair mechanisms. Our findings reveal that migration of normal stem cells in vivo represents an unappreciated source of damage, which could be a significant source of mutations in animals during development or during long-term tissue homeostasis.