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FISH analysis of meiosis in Arabidopsis allopolyploids.

机译:FISH分析拟南芥异倍体中的减数分裂。

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摘要

Although allopolyploids are common in nature and in agriculture, knowledge of their origin, evolution and genomic regulation is limited. We study synthetic allotetraploids of Arabidopsis thaliana and Arabidopsis arenosa as well as the natural allotetraploid Arabidopsis suecica. To elucidate the composition and behavior of the allotetraploid genome, we used chromosome painting with probes from contiguous regions of chromosome 4 of A. thaliana and fluorescent in-situ hybridization with centromeric (CEN) probes specific for each parental genome. We documented the presence of 16 A. arenosa and 10 A. thaliana chromosomes and demonstrate that two different A. arenosa chromosomes are homeologous to chromosome 4 of A. thaliana. Although chromosome pairing in pollen mother cells was predominantly homologous, CENs of different parental origin coalesced at early prophase I, but resolved into proper pairs by metaphase. In addition, CENs of homologous chromosomes were not paired in tapetum cells and endopolyploidy without strict polyteny was evident by the large number of independent CENs. Thus, the Arabidopsis synthetic allopolyploids were capable of homologous pairing as early as three generations after their formation. This indicates that diploid-like pairing is not the result of adaptive mutations in genes that regulate pairing nor the result of structural remodeling of the genomes: rather, it is likely that either the parents provided genes controlling pairing behavior or that features of the parental chromosomes hinder homeologous pairing.
机译:尽管异源多倍体在自然界和农业中很常见,但是对其起源,进化和基因组调控的了解却很有限。我们研究拟南芥和拟南芥合成的异源四倍体以及天然的异源四倍体拟南芥。为了阐明异源四倍体基因组的组成和行为,我们使用了来自拟南芥第4号染色体连续区域的探针进行的染色体涂漆,并与每个亲本基因组特异的着丝粒(CEN)探针进行了荧光原位杂交。我们记录了16个A. arenosa和10个A. thaliana染色体的存在,并证明了两个不同的A. arenosa染色体与A. thaliana的4号染色体同源。尽管花粉母细胞中的染色体配对主要是同源的,但不同亲本来源的CEN在第一阶段的早期就合并了,但是在中期阶段可以分解为适当的配对。此外,在绒毡层细胞中,同源染色体的CEN没有配对,并且通过大量独立的CEN可以证明没有严格多倍性的内多倍体。因此,拟南芥合成的异源多倍体能够在它们形成后的三代之内进行同源配对。这表明二倍体样的配对不是调节配对基因的适应性突变的结果,也不是基因组结构重构的结果:相反,很可能是父母提供了控制配对行为的基因或父母染色体的特征妨碍同源配对。

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