Genome stress response in early development

William F Marzluff; Robert J Duronio

doi:10.1016/j.devcel.2014.05.010

Genome stress response in early development

Dev Cell. 2014 May 27;29(4):375-6. doi: 10.1016/j.devcel.2014.05.010.

Authors

William F Marzluff¹, Robert J Duronio²

Affiliations

¹ Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA; Integrative Program for Biological and Genome Sciences, University of North Carolina, Chapel Hill, NC 27599, USA. Electronic address: william_marzluff@med.unc.edu.
² Departments of Biology and Genetics, University of North Carolina, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA; Integrative Program for Biological and Genome Sciences, University of North Carolina, Chapel Hill, NC 27599, USA. Electronic address: duronio@med.unc.edu.

Abstract

Cells with irreparable genomic damage pose a problem for development and must be eliminated to prevent disease. Reporting in this issue of Developmental Cell, Iampietro et al. (2014) describe a mechanism in Drosophila that removes damaged nuclei from syncytial blastoderm embryos via DNA damage checkpoint kinase-mediated retention of specific mRNAs within the nucleus.

Publication types

Comment

MeSH terms

Animals
Cell Nucleus / genetics*
Checkpoint Kinase 2 / metabolism*
Drosophila Proteins / metabolism*
Drosophila melanogaster / embryology*
RNA-Binding Proteins / metabolism*

Substances

Drosophila Proteins
RNA-Binding Proteins
SLBP protein, Drosophila
Checkpoint Kinase 2
lok protein, Drosophila

Abstract

Publication types

MeSH terms

Substances

Grants and funding