Functional redundancy of two C. elegans homologs of the histone chaperone Asf1 in germline DNA replication

• Published in: Developmental biology 2009-05, Vol.329 (1), p.64-79
• Main Authors: Grigsby, Iwen F., Rutledge, Eric M., Morton, Christine A., Finger, Fern P.
• Format: Article
• Language: English
• Subjects: Animals; Asf1; asfl-1; C. elegans; Caenorhabditis elegans; Caenorhabditis elegans - embryology; Caenorhabditis elegans - genetics; Caenorhabditis elegans - physiology; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - metabolism; Chromatin; Disorders of Sex Development - genetics; DNA Replication; Embryo, Nonmammalian; Female; Gametogenesis; Genes, Helminth; Helminth Proteins - genetics; Helminth Proteins - metabolism; Histones - genetics; Histones - metabolism; In Situ Hybridization; Male; Meiosis; Models, Biological; Molecular Chaperones - genetics; Molecular Chaperones - metabolism; Oogenesis - genetics; Replication; RNA, Messenger - metabolism; Spermatogenesis - genetics; Sterility; unc-85
• ISSN: 0012-1606; 1095-564X
• DOI: 10.1016/j.ydbio.2009.02.015

Eukaryotic genomes contain either one or two genes encoding homologs of the highly conserved histone chaperone Asf1, however, little is known of their in vivo roles in animal development. UNC-85 is one of the two Caenorhabditis elegans Asf1 homologs and functions in post-embryonic replication in neuroblasts. Although UNC-85 is broadly expressed in replicating cells, the specificity of the mutant phenotype suggested possible redundancy with the second C. elegans Asf1 homolog, ASFL-1. The asfl-1 mRNA is expressed in the meiotic region of the germline, and mutants in either Asf1 genes have reduced brood sizes and low penetrance defects in gametogenesis. The asfl-1, unc-85 double mutants are sterile, displaying defects in oogenesis and spermatogenesis, and analysis of DNA synthesis revealed that DNA replication in the germline is blocked. Analysis of somatic phenotypes previously observed in unc-85 mutants revealed that they are neither observed in asfl-1 mutants, nor enhanced in the double mutants, with the exception of enhanced male tail abnormalities in the double mutants. These results suggest that the two Asf1 homologs have partially overlapping functions in the germline, while UNC-85 is primarily responsible for several Asf1 functions in somatic cells, and is more generally involved in replication throughout development.