Are there morphologically abnormal early recombination nodules in the Drosophila melanogaster meiotic mutant mei-218?

Genome ◽  
1989 ◽  
Vol 31 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Adelaide T. C. Carpenter
Keyword(s):  
Drosophila Melanogaster ◽  
Synaptonemal Complex ◽  
Gene Conversion ◽  
Meiotic Recombination ◽  
Cytological Study ◽  
Specific Probe ◽  
Definitive Answer ◽  
Recombination Nodules ◽  
Defective Mutant ◽  
Meiotic Crossover

Early recombination nodules have been suggested to perform a role in meiotic gene conversion recombination events. The meiotic recombination-defective mutant mei-218 greatly reduces the frequency of meiotic crossover (reciprocal) recombination events and reduces the number of late recombination nodules to the same extent. However, it does not reduce the frequency of simple gene conversion events, although they are abnormal in having shorter coconversion tracts than controls. The original cytological study yielded somewhat fewer early nodules in mei-218 than in controls, although very abnormal ones might have been missed. The present study failed to identify a mei-218 specific abnormal category. However, because recombination nodules are at present recognizable only by their morphology, a definitive answer to this question must await a specific probe for recombination nodules. Moreover, the possibility remains that early nodules in mei-218 are more ephemeral than are early nodules in wild type.Key words: synaptonemal complex, recombination nodules, meiotic mutants, Drosophila melanogaster.

scholarly journals SYNAPTONEMAL COMPLEX AND RECOMBINATION NODULES IN WILD-TYPE DROSOPHILA MELANOGASTER FEMALES

Genetics ◽  
1979 ◽  
Vol 92 (2) ◽  
pp. 511-541
Author(s):  
Adelaide T C Carpenter
Keyword(s):  
Drosophila Melanogaster ◽  
Synaptonemal Complex ◽  
Meiotic Recombination ◽  
Morphological Type ◽  
Wild Type ◽  
Recombination Nodule ◽  
Recombination Nodules ◽  
Recombination Processes ◽  
A Subunit ◽  
Serial Section Reconstruction

ABSTRACT Electron microscope serial section reconstruction analysis of all zygotene-pachytene nuclei of meiotic cells from three wild-type germaria (a subunit of the ovary containing the early meiotic stages arrayed in temporal developmental sequence) of Drosophila melanogaster females corroborates and extends earlier observations (CARPENTER 1975a) on the nature and sequence of ultrastructural events occurring during the time of meiotic recombination. Emphasis has been placed on (1) the time of appearance and disappearance of the synaptonemal complex (SC) and the changes in its dimensions that accompany a cell's progression through pachytene, and (2) the appearance, disappearance, number and chromosomal locations of recombination nodules (CARPENTER 1975b). For both the SC and the recombination nodule the availability of several developmental series has provided an estimate of the biological variability in the properties of these recombination-associated structures. The much more extensive data presented here substantiate the earlier hypothesis that recombination nodules occur at sites where reciprocal meiotic recombination will occur, has occurred, or is occurring. A second morphological type of recombination nodule is reported; it is suggested that the presence of the latter type of nodule may correlate with sites of gene conversion. The hypothesis that there may be two types of meiotic recombination processes is discussed.

scholarly journals Crossover patterning through kinase-regulated condensation and coarsening of recombination nodules

2021 ◽  
Author(s):  
Liangyu Zhang ◽  
Weston Stauffer ◽  
David Zwicker ◽  
Abby F. Dernburg
Keyword(s):  
Synaptonemal Complex ◽  
Meiotic Recombination ◽  
Ring Domain ◽  
Homologous Chromosomes ◽  
Crossover Interference ◽  
C Elegans ◽  
Recombination Nodules

AbstractMeiotic recombination is highly regulated to ensure precise segregation of homologous chromosomes. Evidence from diverse organisms indicates that the synaptonemal complex (SC), which assembles between paired chromosomes, plays essential roles in crossover formation and patterning. Several additional “pro-crossover” proteins are also required for recombination intermediates to become crossovers. These typically form multiple foci or recombination nodules along SCs, and later accumulate at fewer, widely spaced sites. Here we report that in C. elegans CDK-2 is required to stabilize all crossover intermediates and stabilizes interactions among pro-crossover factors by phosphorylating MSH-5. Additionally, we show that the conserved RING domain proteins ZHP-3/4 diffuse along the SC and remain dynamic following their accumulation at recombination sites. Based on these and previous findings we propose a model in which recombination nodules arise through spatially restricted biomolecular condensation and then undergo a regulated coarsening process, resulting in crossover interference.

Solitary and synaptonemal complex-associated recombination nodules in pro-nurse cells during oogenesis in Drosophila melanogaster

Chromosoma ◽  
1993 ◽  
Vol 102 (6) ◽  
pp. 396-402 ◽  
Author(s):  
Karin Schmekel ◽  
Jacob Wahrman ◽  
Bertil Daneholt
Keyword(s):  
Drosophila Melanogaster ◽  
Synaptonemal Complex ◽  
Nurse Cells ◽  
Recombination Nodules

scholarly journals A Role for Synaptonemal Complex in Meiotic Mismatch Repair

Genetics ◽  
2021 ◽  
Author(s):  
Karen Voelkel-Meiman ◽  
Ashwini Oke ◽  
Arden Feil ◽  
Alexander Shames ◽  
Jennifer Fung ◽  
...  
Keyword(s):  
Synaptonemal Complex ◽  
Gene Conversion ◽  
Mismatch Repair ◽  
Meiotic Recombination ◽  
High Throughput Sequencing ◽  
Central Element ◽  
Similar Degree ◽  
Meiotic Segregation ◽  
Wild Type ◽  
A Genome

Abstract A large subset of meiotic recombination intermediates form within the physical context of synaptonemal complex (SC), but the functional relationship between SC structure and homologous recombination remains obscure. Our prior analysis of strains deficient for SC central element proteins demonstrated that tripartite SC is dispensable for interhomolog recombination in S. cerevisiae. Here we report that while dispensable for recombination per se, SC proteins promote efficient mismatch repair at interhomolog recombination sites. Failure to repair mismatches within heteroduplex-containing meiotic recombination intermediates leads to genotypically sectored colonies (post meiotic segregation events). We discovered increased post-meiotic segregation at THR1 in cells lacking Ecm11 or Gmc2, or in the SC-deficient but recombination-proficient zip1[Δ21-163] mutant. High-throughput sequencing of octad meiotic products furthermore revealed a genome-wide increase in recombination events with unrepaired mismatches in ecm11 mutants relative to wild type. Meiotic cells missing Ecm11 display longer gene conversion tracts, but tract length alone does not account for the higher frequency of unrepaired mismatches. Interestingly, the per-nucleotide mismatch frequency is elevated in ecm11 when analyzing all gene conversion tracts, but is similar between wild type and ecm11 if considering only those events with unrepaired mismatches. Thus, in both wild type and ecm11 strains a subset of recombination events is susceptible to a similar degree of inefficient mismatch repair, but in ecm11 mutants a larger fraction of events fall into this inefficient repair category. Finally, we observe elevated post-meiotic segregation at THR1 in mutants with a dual deficiency in MutSγ crossover recombination and SC assembly, but not in the mlh3 mutant, which lacks MutSγ crossovers but has abundant SC. We propose that SC structure promotes efficient mismatch repair of joint molecule recombination intermediates, and that absence of SC is the molecular basis for elevated post-meiotic segregation in both MutSγ crossover-proficient (ecm11, gmc2) and MutSγ crossover-deficient (msh4, zip3) strains.

Recombination nodules and synaptonemal complex in recombination-defective females of Drosophila melanogaster

Chromosoma ◽  
1979 ◽  
Vol 75 (3) ◽  
pp. 259-292 ◽  
Author(s):  
Adelaide T. C. Carpenter
Keyword(s):  
Drosophila Melanogaster ◽  
Synaptonemal Complex ◽  
Recombination Nodules

Normal Synaptonemal Complex and Abnormal Recombination Nodules in Two Alleles of the Drosophila Meiotic Mutant mei-W68

Genetics ◽  
2003 ◽  
Vol 163 (4) ◽  
pp. 1337-1356 ◽  
Author(s):  
Adelaide T C Carpenter
Keyword(s):  
Electron Microscopy ◽  
Synaptonemal Complex ◽  
High Frequency ◽  
Serial Section ◽  
The Other ◽  
Wild Type ◽  
Recombination Nodules ◽  
Section Electron ◽  
Serial Section Electron Microscopy ◽  
Section Electron Microscopy

Abstract The meiotic phenotypes of two mutant alleles of the mei-W68 gene, 1 and L1, were studied by genetics and by serial-section electron microscopy. Despite no or reduced exchange, both mutant alleles have normal synaptonemal complex. However, neither has any early recombination nodules; instead, both exhibit high numbers of very long (up to 2 μm) structures here named “noodles.” These are hypothesized to be formed by the unchecked extension of identical but much shorter structures ephemerally seen in wild type, which may be precursors of early recombination nodules. Although the mei-W68L1 allele is identical to the mei-W681 allele in both the absence of early recombination nodules and a high frequency of noodles (i.e., it is amorphic for the noodle phene), it is hypomorphic in its effects on exchange and late recombination nodules. The differential effects of this allele on early and late recombination nodules are consistent with the hypothesis that Drosophila females have two separate recombination pathways—one for simple gene conversion, the other for exchange.

scholarly journals The Pif1 helicase is actively inhibited during meiotic recombination which restrains gene conversion tract length

2021 ◽  
Author(s):  
Dipti Vinayak Vernekar ◽  
Giordano Reginato ◽  
Céline Adam ◽  
Lepakshi Ranjha ◽  
Florent Dingli ◽  
...  
Keyword(s):  
Gene Conversion ◽  
Meiotic Recombination ◽  
Strand Break ◽  
Dna Helicase ◽  
Clamp Loader ◽  
Repair Synthesis ◽  
Dna Repair Synthesis ◽  
Gene Conversions

Abstract Meiotic recombination ensures proper chromosome segregation to form viable gametes and results in gene conversions events between homologs. Conversion tracts are shorter in meiosis than in mitotically dividing cells. This results at least in part from the binding of a complex, containing the Mer3 helicase and the MutLβ heterodimer, to meiotic recombination intermediates. The molecular actors inhibited by this complex are elusive. The Pif1 DNA helicase is known to stimulate DNA polymerase delta (Pol δ) -mediated DNA synthesis from D-loops, allowing long synthesis required for break-induced replication. We show that Pif1 is also recruited genome wide to meiotic DNA double-strand break (DSB) sites. We further show that Pif1, through its interaction with PCNA, is required for the long gene conversions observed in the absence of MutLβ recruitment to recombination sites. In vivo, Mer3 interacts with the PCNA clamp loader RFC, and in vitro, Mer3-MutLβ ensemble inhibits Pif1-stimulated D-loop extension by Pol δ and RFC-PCNA. Mechanistically, our results suggest that Mer3-MutLβ may compete with Pif1 for binding to RFC-PCNA. Taken together, our data show that Pif1’s activity that promotes meiotic DNA repair synthesis is restrained by the Mer3-MutLβ ensemble which in turn prevents long gene conversion tracts and possibly associated mutagenesis.

The Effect of Heterologous Insertions on Gene Conversion in Mitotically Dividing Cells in Drosophila melanogaster

Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 249-258
Author(s):  
Angela M Coveny ◽  
Tammy Dray ◽  
Gregory B Gloor
Keyword(s):  
Drosophila Melanogaster ◽  
Gene Conversion ◽  
Strand Break ◽  
Double Strand Break ◽  
P Element ◽  
Double Strand Break Repair ◽  
Break Site ◽  
In Trans ◽  
Break Repair ◽  
In Cis

Abstract We examined the influence that heterologous sequences of different sizes have on the frequency of double-strand-break repair by gene conversion in Drosophila melanogaster. We induced a double-strand break on one X chromosome in female flies by P-element excision. These flies contained heterologous insertions of various sizes located 238 bp from the break site in cis or in trans to the break, or both. We observed a significant decrease in double-strand-break repair with large heterologous insertions located either in cis or in trans to the break. Reestablishing the homology by including the same heterologous sequence in cis and in trans to the double-strand break restored the frequency of gene conversion to wild-type levels. In one instance, an allelic nonhomologous insertion completely abolished repair by homologous recombination. The results show that the repair of a double-strand break by gene conversion requires chromosome pairing in the local region of the double-strand break.

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