Effect of the Pairing Gene Ph1 and Premeiotic Colchicine Treatment on Intra- and Interchromosome Pairing of Isochromosomes in Common Wheat

Genetics ◽  
1998 ◽  
Vol 150 (3) ◽  
pp. 1199-1208 ◽  
Author(s):  
Juan M Vega ◽  
Moshe Feldman

Abstract The analysis of the pattern of isochromosome pairing allows one to distinguish factors affecting presynaptic alignment of homologous chromosomes from those affecting synapsis and crossing-over. Because the two homologous arms in an isochromosome are invariably associated by a common centromere, the suppression of pairing between these arms (intrachromosome pairing) would indicate that synaptic or postsynaptic events were impaired. In contrast, the suppression of pairing between an isochromosome and its homologous chromosome (interchromosome pairing), without affecting intrachromosome pairing, would suggest that homologous presynaptic alignment was impaired. We used such an isochromosome system to determine which of the processes associated with chromosome pairing was affected by the Ph1 gene of common wheat—the main gene that restricts pairing to homologues. Ph1 reduced the frequency of interchromosome pairing without affecting intrachromosome pairing. In contrast, intrachromosome pairing was strongly reduced in the absence of the synaptic gene Syn-B1. Premeiotic colchicine treatment, which drastically decreased pairing of conventional chromosomes, reduced interchromosome but not intrachromosome pairing. The results support the hypothesis that premeiotic alignment is a necessary stage for the regularity of meiotic pairing and that Ph1 relaxes this alignment. We suggest that Ph1 acts on premeiotic alignment of homologues and homeologues as a means of ensuring diploid-like meiotic behavior in polyploid wheat.

Genetics ◽  
1998 ◽  
Vol 148 (3) ◽  
pp. 1285-1294
Author(s):  
Juan M Vega ◽  
Moshe Feldman

Abstract The cytologically diploid-like meiotic behavior of hexaploid wheat (i.e., exclusive bivalent pairing of homologues) is largely controlled by the pairing homoeologous gene Ph1. This gene suppresses pairing between homoeologous (partially homologous) chromosomes of the three closely related genomes that compose the hexaploid wheat complement. It has been previously proposed that Ph1 regulates meiotic pairing by determining the pattern of premeiotic arrangement of homologous and homoeologous chromosomes. We therefore assume that Ph1 action may be targeted at the interaction of centromeres with spindle microtubules—an interaction that is critical for movement of chromosomes to their specific interphase positions. Using monosomic lines of common wheat, we studied the effect of this gene on types and rates of centromere division of univalents at meiosis. In the presence of the normal two doses of Ph1, the frequency of transverse breakage (misdivision) of the centromere of univalent chromosomes was high in both first and second meiotic divisions; whereas with zero dose of the gene, this frequency was drastically reduced. The results suggest that Ph1 is a trans-acting gene affecting centromere-microtubules interaction. The findings are discussed in the context of the effect of Ph1 on interphase chromosome arrangement.


Science ◽  
2017 ◽  
Vol 355 (6323) ◽  
pp. 408-411 ◽  
Author(s):  
Jasvinder S. Ahuja ◽  
Rima Sandhu ◽  
Rana Mainpal ◽  
Crystal Lawson ◽  
Hanna Henley ◽  
...  

During meiosis, paired homologous chromosomes (homologs) become linked via the synaptonemal complex (SC) and crossovers. Crossovers mediate homolog segregation and arise from self-inflicted double-strand breaks (DSBs). Here, we identified a role for the proteasome, the multisubunit protease that degrades proteins in the nucleus and cytoplasm, in homolog juxtaposition and crossing over. Without proteasome function, homologs failed to pair and instead remained associated with nonhomologous chromosomes. Although dispensable for noncrossover formation, a functional proteasome was required for a coordinated transition that entails SC assembly between longitudinally organized chromosome axes and stable strand exchange of crossover-designated DSBs. Notably, proteolytic core and regulatory proteasome particles were recruited to chromosomes by Zip3, the ortholog of mammalian E3 ligase RNF212, and SC protein Zip1 . We conclude that proteasome functions along meiotic chromosomes are evolutionarily conserved.


1976 ◽  
Vol 18 (4) ◽  
pp. 731-738 ◽  
Author(s):  
Lydia Avivi

The low-pairing gene or genes of diploid Triticum longissimum (Schwinf. &Muschl.) Bowden predispose the induced autotetraploid towards bivalent pairing. In this work, bivalentization was phenocopied in intermediate- and low-pairing lines of T. longissimum and in a high-pairing line of T. speltoides (Tausch) Gren. ex Richter, by colchicine treatment during the last premeiotic mitosis. This treatment induced C-mitosis and tetraploid cells which are characterized by almost exclusive bivalent pairing instead of the expected multivalent pairing. Colchicine disrupted the association of homologous chromosomes in the premeiotic metaphase but left the sister chromatids located close to each other. As a result, rather than being all closely associated, the four homologues were arranged in pairs already prior to meiosis. The effect of colchicine in this respect is reminiscent of that of the "diploidizing genes" in many naturally occurring polyploids. This work demonstrates once again the significance which the pattern of premeiotic homologous association has for the manner of meiotic pairing.


Genome ◽  
2004 ◽  
Vol 47 (2) ◽  
pp. 399-403 ◽  
Author(s):  
Maria Vorontsova ◽  
Peter Shaw ◽  
Steve Reader ◽  
Graham Moore

Both homologous and non-homologous chromosomes in wheat associate via their centromeric hetero chromatin in the developing xylem vessel cells of the root. The antimetabolite 5-azacytidine (which reduces DNA methylation) decreases the overall level of centromere association. Treatment with 5-azacytidine caused a more marked reduction in the level of homologous chromosome association observed in a wheat line carrying a pair of marked chromosomes. On the other hand, treatment of wheat seedlings with trichostatin A (which increases histone acetylation) raises the overall level of centromere association. The Ph1 locus controls the specificity of both somatic and meiotic pairing of homologous centromeres in wheat. The level of non-homologously associated centromeres is, however, reduced in the presence of Ph1 compared with its absence, even after treatment with either drug. Thus these two drugs, which have been shown to affect chromatin structure, do affect chromosome association, but Ph1 must act at least in part by a different mechanism.Key words: pairing, roots, cereals, Ph1, polyploids.


Genetics ◽  
1990 ◽  
Vol 126 (1) ◽  
pp. 167-176
Author(s):  
D Gubb ◽  
M Ashburner ◽  
J Roote ◽  
T Davis

Abstract The zeste mutation of Drosophila melanogaster suppresses the expression of white genes in the eye. This suppression is normally dependent on there being two copies of w+ located close to each other in the genome--they may either be in cis (as in a tandem duplication of w+) or in trans, i.e. on homologous chromosomes. Duplicated w+ genes carried by a giant transposing element, TE146(Z), are suppressed by z whether they are in direct (tandem) or inverted order. The tandem form of the TE is very sensitive to a rearrangement on the homologous chromosome--many rearrangements with breakpoints "opposite" the TE's insertion site prevent the interaction between the white genes on a z background. These aberrations act as dominant suppressors of zeste that are specific to the tandemly duplicated form of TE146(Z). The inverted form of the TE146(Z) presumably pairs as a hairpin loop; this is more stable than the tandem form by the criterion that its zeste phenotype is unaffected by any of the aberrations. This effect of rearrangements has been used as the basis for a screen, gamma-ray induced aberrations with at least one breakpoint opposite the TE site were recovered by their suppression of the zeste phenotype.


Author(s):  
Shisheng Chen ◽  
Joshua Hegarty ◽  
Tao Shen ◽  
Lei Hua ◽  
Hongna Li ◽  
...  

AbstractKey messageThe stripe rust resistance geneYr34 was transferred to polyploid wheat chromosome 5AL from T. monococcumand has been used for over two centuries.Wheat stripe (or yellow) rust, caused by Puccinia striiformis f. sp. tritici (Pst), is currently among the most damaging fungal diseases of wheat worldwide. In this study, we report that the stripe rust resistance gene Yr34 (synonym Yr48) is located within a distal segment of the cultivated Triticum monococcum subsp. monococcum chromosome 5AmL translocated to chromosome 5AL in polyploid wheat. The diploid wheat species Triticum monococcum (genome AmAm) is closely related to T. urartu (donor of the A genome to polyploid wheat) and has good levels of resistance against the stripe rust pathogen. When present in hexaploid wheat, the T. monococcum Yr34 resistance gene confers a moderate level of resistance against virulent Pst races present in California and the virulent Chinese race CYR34. In a survey of 1,442 common wheat genotypes, we identified 5AmL translocations of fourteen different lengths in 17.5% of the accessions, with higher frequencies in Europe than in other continents. The old European wheat variety “Mediterranean” was identified as a putative source of this translocation, suggesting that Yr34 has been used for over 200 years. Finally, we designed diagnostic CAPS and sequenced-based markers that will be useful to accelerate the deployment of Yr34 in wheat breeding programs to improve resistance to this devastating pathogen.


Genome ◽  
1992 ◽  
Vol 35 (1) ◽  
pp. 140-146 ◽  
Author(s):  
R. J. Singh ◽  
K. P. Kollipara ◽  
F. Ahmad ◽  
T. Hymowitz

The objective of this study was to discover the diploid progenitors of 80-chromosome Glycine tabacina with adventitious roots (WAR) and no adventitious roots (NAR). Three synthetic amphiploids were obtained by somatic chromosome doubling. These were (i) (G. latifolia, 2n = 40, genome B1B1,) × (G. microphylla, 2n = 40, genome BB) = F1(2n = 40, genome BB1) – 0.1% colchicine treatment (CT) – 2n = 80, genome BBB1B1; (ii) (G. canescens, 2n = 40, genome AA) × G. microphylla, 2n = 40, genome BB) = F1 (2n = 40, genome AB) – (CT) – 2n = 80, genome AABB; (iii) (G. latifolia, 2n = 40, B1B1) × G. canescens, 2n = 40, AA) = F1 (2n = 40, genome AB1) – (CT) – 2n = 80, genome AAB1B1. The segmental allotetraploid BBB1B1 was morphologically similar to the 80-chromosome G. tabacina (WAR), but meiotic pairing data in F1 hybrids did not support the complete genomic affinity. Despite normal diploid-like meiosis in allotetraploids AABB and AAB1B1, AABB was completely fertile, while pod set in AAB1B1 was very sparse. Morphologically, allotetraploid AABB was indistinguishable from the 80-chromosome G. tabacina (NAR) but in their F1 hybrids, the range of univalents at metaphase I was wide (4–44). The allotetraploid AAB1B1 did not morphologically resemble the 80-chromosome G. tabacina (NAR). However, the F1 hybrid of AABB × AAB1B1 showed normal meiosis with an average chromosome association (range) of 1.7 I (0–4) + 39.2 II (38–40). Based on this information, we cannot correctly deduce the diploid progenitor species of the 80-chromosome G. tabacina (NAR). The lack of exact genome homology may be attributed to the geographical isolation, natural mutation, and growing environmental conditions since the inception of 80-chromosome G. tabacina. Thus, it is logical to suggest that the 80-chromosome G. tabacina (NAR) is a complex, probably synthesized from A genome (G. canescens, G. clandestina, G. argyrea, G. tomentella D4 isozyme group) and B genome (G. latifolia, G. microphylla, G. tabacina) species, and the 80-chromosome G. tabacina (WAR) complex was evolved through segmental allopolyploidy from the B genome species.Key words: Glycine spp., allopolyploidy, colchicine, genome, intra- and inter-specific hybridization, polyploid complex.


Meiotic chromosome pairing is a process that is amenable to genetic and experimental analysis. The combined use of these two approaches allows for the process to be dissected into several finite periods of time in which the developmental stages of pairing can be precisely located. Evidence is now available, in particular in plants, that shows that the pairing of homologous chromosomes, as observed at metaphase I, is affected by events occurring as early as the last premeiotic mitosis; and that the maintenance of this early determined state is subsequently maintained by constituents (presumably proteins) that are sensitive to either colchicine, temperature or gene control. A critical assessment of this evidence in wheat and a comparison of the process of pairing in wheat with the course of meiotic pairing in other plants and animals is presented.


1972 ◽  
Vol 14 (2) ◽  
pp. 397-401 ◽  
Author(s):  
Kathleen Church

Chromosome behaviour occurring from premeiotic DNA synthesis to leptotene of meiosis is described for both males (spermatogenesis) and females (oogenesis) in the grasshopper Melanoplus femur-rubrum. These events include a period of chromosome spiralization and contraction following premeiotic DNA synthesis and prior to leptotene. The diploid complement of chromosomes becomes visible in both sexes. No pairing between homologous chromosomes or chiasmata are observed in either sex. The results suggest that synapsis and crossing over must occur following preleptotene spiralization during spermatogenesis and oogenesis in this grasshopper.


2017 ◽  
Vol 216 (2) ◽  
pp. 393-408 ◽  
Author(s):  
Benjamin Alleva ◽  
Nathan Balukoff ◽  
Amy Peiper ◽  
Sarit Smolikove

In meiotic prophase I, homologous chromosome pairing is promoted through chromosome movement mediated by nuclear envelope proteins, microtubules, and dynein. After proper homologue pairing has been established, the synaptonemal complex (SC) assembles along the paired homologues, stabilizing their interaction and allowing for crossing over to occur. Previous studies have shown that perturbing chromosome movement leads to pairing defects and SC polycomplex formation. We show that FKB-6 plays a role in SC assembly and is required for timely pairing and proper double-strand break repair kinetics. FKB-6 localizes outside the nucleus, and in its absence, the microtubule network is altered. FKB-6 is required for proper movement of dynein, increasing resting time between movements. Attenuating chromosomal movement in fkb-6 mutants partially restores the defects in synapsis, in agreement with FKB-6 acting by decreasing chromosomal movement. Therefore, we suggest that FKB-6 plays a role in regulating dynein movement by preventing excess chromosome movement, which is essential for proper SC assembly and homologous chromosome pairing.


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