Presentation/Session Information

Session Information

Session Title: RNA Interference, Noncoding RNAs, and Genetic Technologies Session Type: Parallel
Session Location: Carnesale Palisades Ballroom Session Time: Sat, Jun 27 8:30AM - 11:30AM

Presentation Information

Program Number: 145 Presentation Time: 10:18AM - 10:30AM

Presentation Content

Homologous pairing and unpaired silencing of chromosomes are regulated by RNAi during meiosis in C. elegans.Hiroaki Tabara 1,2, Shohei Mitani 3, Megumi Mochizuki 4, Yuji Kohara 2, Kyosuke Nagata 1. 1)University of Tsukuba, Fac. of Medicine, Japan; 2)National Institute of Genetics; 3)Tokyo Women's Med. Univ.; 4)Kyoto Univ.

  During meiosis, most chromosomes have homologous partners and undergo homologous pairing.  In contrast, pairing does not occur for X-chromosomes in males of C. elegans and free-type chromosome duplications.  These unpaired chromosomes are heterochromatinized by meiotic silencing of unpaired DNA, which is often abbreviated to meiotic silencing.  We analyzed the differences and similarities of regulation of paired and unpaired chromosomes during meiosis.
  In C. elegans, unpaired DNA subjected to meiotic silencing forms facultative heterochromatin that is rich in dimethylation of lysine 9 on histone H3 (H3K9me2).  Heterochromatinization of unpaired chromosome is known to be abnormal in some RNAi mutants, such as the csr-1 mutant corresponding to an Argonaute protein, which has an RNA cleavage (Slicer) activity in conjunction with triphosphorylated siRNAs produced by RNA-dependent RNA polymerases.  A similar Slicer activity was detected also from C04F12.1 corresponding to another Argonaute protein.  We found that C04F12.1(tm1637) mutation enhanced the meiotic silencing defect caused by csr-1(fj54) mutation.  While endogenous RNAi is thought to be involved in the early phase of meiotic silencing, the nature of heterochromatin formed by meiotic silencing is not well understood.  Our biochemical analysis identified a chromo-domain protein CEC-5 as a component of heterochromatin formed by meiotic silencing.  Triple-mutations of cec-5 and similar genes significantly diminished H3K9me2 signals thought to correspond to unpaired chromosomes.  In addition, we found that the activity of meiosis-specific cohesin containing COH-3/4 kleisin is required for meiotic silencing.  Our immunostaining detected COH-3/4 on unpaired chromosomes and at lateral axes of the synaptonemal complex on paired chromosomes.
  Considering the distribution of COH-3/4, we next asked whether mutants corresponding to COH-3/4 and Slicer-type Argonaute proteins show any defect in homolog pairing.  As results of immunofluorescence and FISH experiments, the coh-3/4 double-mutant and the Slicer-type Argonaute double-mutant showed the defects in homolog pairing, except for pairing centers.  An abnormal distribution of COH-3/4 was also observed in some gonads of the Argonaute double-mutant.  Slicer-type Argonaute proteins are not essential for axis formation of the synaptonemal complex, but they are necessary for formation of a synaptonemal complex with accurate homology between homologous chromosomes.
  Thus, mechanisms of RNAi, meiotic silencing and homologous pairing overlap partially with each other in this organism.




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