PMID- 26984058 OWN - NLM STAT- MEDLINE DCOM- 20170223 LR - 20181202 IS - 1943-2631 (Electronic) IS - 0016-6731 (Print) IS - 0016-6731 (Linking) VI - 203 IP - 1 DP - 2016 May TI - Heterochromatin-Associated Proteins HP1a and Piwi Collaborate to Maintain the Association of Achiasmate Homologs in Drosophila Oocytes. PG - 173-89 LID - 10.1534/genetics.115.186460 [doi] AB - Accurate segregation of homologous chromosomes during meiosis depends on their ability to remain physically connected throughout prophase I. For homologs that achieve a crossover, sister chromatid cohesion distal to the chiasma keeps them attached until anaphase I. However, in Drosophila melanogaster wild-type oocytes, chromosome 4 never recombines, and the X chromosome fails to cross over in 6-10% of oocytes. Proper segregation of these achiasmate homologs relies on their pericentric heterochromatin-mediated association, but the mechanism(s) underlying this attachment remains poorly understood. Using an inducible RNA interference (RNAi) strategy combined with fluorescence in situ hybridization (FISH) to monitor centromere proximal association of the achiasmate FM7a/X homolog pair, we asked whether specific heterochromatin-associated proteins are required for the association and proper segregation of achiasmate homologs in Drosophila oocytes. When we knock down HP1a, H3K9 methytransferases, or the HP1a binding partner Piwi during mid-prophase, we observe significant disruption of pericentric heterochromatin-mediated association of FM7a/X homologs. Furthermore, for both HP1a and Piwi knockdown oocytes, transgenic coexpression of the corresponding wild-type protein is able to rescue RNAi-induced defects, but expression of a mutant protein with a single amino acid change that disrupts the HP1a-Piwi interaction is unable to do so. We show that Piwi is stably bound to numerous sites along the meiotic chromosomes, including centromere proximal regions. In addition, reduction of HP1a or Piwi during meiotic prophase induces a significant increase in FM7a/X segregation errors. We present a speculative model outlining how HP1a and Piwi could collaborate to keep achiasmate chromosomes associated in a homology-dependent manner. CI - Copyright (c) 2016 by the Genetics Society of America. FAU - Giauque, Christopher C AU - Giauque CC AD - Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755. FAU - Bickel, Sharon E AU - Bickel SE AD - Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755 sharon.e.bickel@dartmouth.edu. LA - eng GR - P40 OD010949/OD/NIH HHS/United States GR - P40 OD018537/OD/NIH HHS/United States GR - R01 GM059354/GM/NIGMS NIH HHS/United States GR - R01 GM084947/GM/NIGMS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20160316 PL - United States TA - Genetics JT - Genetics JID - 0374636 RN - 0 (Argonaute Proteins) RN - 0 (Chromosomal Proteins, Non-Histone) RN - 0 (DNA-Binding Proteins) RN - 0 (Drosophila Proteins) RN - 0 (Histones) RN - 0 (heterochromatin protein 1, Drosophila) RN - 0 (piwi protein, Drosophila) RN - EC 2.1.1.- (Histone Methyltransferases) RN - EC 2.1.1.43 (Histone-Lysine N-Methyltransferase) SB - IM MH - Animals MH - Argonaute Proteins/*metabolism MH - Chromosomal Proteins, Non-Histone/genetics/*metabolism MH - Chromosome Segregation MH - DNA-Binding Proteins MH - Drosophila/*genetics/*metabolism MH - Drosophila Proteins/genetics/*metabolism MH - Female MH - Gene Knockdown Techniques MH - Histone Methyltransferases MH - Histone-Lysine N-Methyltransferase/metabolism MH - Histones/metabolism MH - Meiosis MH - Mutation MH - Nondisjunction, Genetic MH - Oocytes/*metabolism MH - Protein Binding PMC - PMC4858772 OTO - NOTNLM OT - *H3K9 methyltransferases OT - *chromosome segregation OT - *meiosis OT - *nondisjunction OT - *pericentric heterochromatin EDAT- 2016/03/18 06:00 MHDA- 2017/02/24 06:00 PMCR- 2017/05/01 CRDT- 2016/03/18 06:00 PHST- 2015/12/22 00:00 [received] PHST- 2016/03/11 00:00 [accepted] PHST- 2016/03/18 06:00 [entrez] PHST- 2016/03/18 06:00 [pubmed] PHST- 2017/02/24 06:00 [medline] PHST- 2017/05/01 00:00 [pmc-release] AID - genetics.115.186460 [pii] AID - 186460 [pii] AID - 10.1534/genetics.115.186460 [doi] PST - ppublish SO - Genetics. 2016 May;203(1):173-89. doi: 10.1534/genetics.115.186460. Epub 2016 Mar 16.