Translate this page to:
In JoVE (1)
Other Publications (2)
Articles by Connie Hajjar in JoVE
Time-lapse Microscopy of Early Embryogenesis in Caenorhabditis elegans
Lynn Boyd1, Connie Hajjar1, Kevin O'Connell2
1Department of Biological Sciences, University of Alabama in Huntsville, 2NIDDK-National Institutes of Health
This article describes a technique for the visualization of the early events of embryogenesis in the nematode Caenorhabditis elegans.
Other articles by Connie Hajjar on PubMed
Ubiquitin Conjugating Enzymes Participate in Polyglutamine Protein Aggregation
BMC Cell Biology. 2007 | Pubmed ID: 17663792
Protein aggregation is a hallmark of several neurodegenerative diseases including Huntington's disease and Parkinson's disease. Proteins containing long, homopolymeric stretches of glutamine are especially prone to form aggregates. It has long been known that the small protein modifier, ubiquitin, localizes to these aggregates. In this report, nematode and cell culture models for polyglutamine aggregation are used to investigate the role of the ubiquitin pathway in protein aggregation.
Postfertilization Autophagy of Sperm Organelles Prevents Paternal Mitochondrial DNA Transmission
Science (New York, N.Y.). Nov, 2011 | Pubmed ID: 22033522
In sexual reproduction of most animals, the spermatozoon provides DNA and centrioles, together with some cytoplasm and organelles, to the oocyte that is being fertilized. Paternal mitochondria and their genomes are generally eliminated in the embryo by an unknown degradation mechanism. We show that, upon fertilization, a Caenorhabditis elegans spermatozoon triggers the recruitment of autophagosomes within minutes and subsequent paternal mitochondria degradation. Whereas the nematode-specific sperm membranous organelles are ubiquitinated before autophagosome formation, the mitochondria are not. The degradation of both paternal structures and mitochondrial DNA requires an LC3-dependent autophagy. Analysis of fertilized mouse embryos shows the localization of autophagy markers, which suggests that this autophagy event is evolutionarily conserved to prevent both the transmission of paternal mitochondrial DNA to the offspring and the establishment of heteroplasmy.
