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涉及 atp9 基因的重组事件与向日葵 CMS PET2 的雄性不育有关。

Recombination Events Involving the atp9 Gene Are Associated with Male Sterility of CMS PET2 in Sunflower.

机构信息

Institut für Biowissenschaften, Abt. Pflanzengenetik, Universität Rostock, Albert-Einstein-Straße 3, D-18059 Rostock, Germany.

出版信息

Int J Mol Sci. 2018 Mar 11;19(3):806. doi: 10.3390/ijms19030806.

DOI:10.3390/ijms19030806
PMID:29534485
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5877667/
Abstract

Cytoplasmic male sterility (CMS) systems represent ideal mutants to study the role of mitochondria in pollen development. In sunflower, CMS PET2 also has the potential to become an alternative CMS source for commercial sunflower hybrid breeding. CMS PET2 originates from an interspecific cross of and as CMS PET1, but results in a different CMS mechanism. Southern analyses revealed differences for , and between CMS PET2, CMS PET1 and the male-fertile line HA89. A second identical copy of was present on an additional CMS PET2-specific fragment. In addition, the gene was duplicated. However, this duplication was followed by an insertion of 271 bp of unknown origin in the 5' coding region of the gene in CMS PET2, which led to the creation of two unique open reading frames and . The first 53 bp of are identical to the 5' end of . consists apart from the first 3 bp, being part of the 271-bp-insertion, of the last 228 bp of . These CMS PET2-specific orfs are co-transcribed. All 11 editing sites of the gene present in are fully edited. The anther-specific reduction of the co-transcript in fertility-restored hybrids supports the involvement in male-sterility based on CMS PET2.

摘要

细胞质雄性不育(CMS)系统是研究线粒体在花粉发育中的作用的理想突变体。在向日葵中,CMS PET2 也有可能成为商业向日葵杂交种培育的替代 CMS 来源。CMS PET2 源自 和 之间的种间杂交作为 CMS PET1,但导致了不同的 CMS 机制。南方分析显示 CMS PET2、CMS PET1 和雄性可育系 HA89 之间在 、 和 上存在差异。第二个相同的 拷贝存在于 CMS PET2 特有的额外片段上。此外, 基因被复制。然而,在 CMS PET2 的 基因 5'编码区插入了 271bp 的未知来源,导致了两个独特的开放阅读框 和 的产生。 的前 53bp 与 的 5'端相同。 除了前 3bp 外,还包含 271bp 插入的最后 228bp 。这些 CMS PET2 特有的 orfs 是共转录的。 在 中存在的 基因的 11 个编辑位点均完全编辑。在可育恢复杂种中,转录本在花药中的特异性减少支持了基于 CMS PET2 的雄性不育的参与。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/8ebcfa3b2d60/ijms-19-00806-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/c1f367dd6788/ijms-19-00806-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/72e722ef401c/ijms-19-00806-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/125c9af4da2e/ijms-19-00806-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/175610421b3d/ijms-19-00806-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/20dfe20a5312/ijms-19-00806-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/a1d2e32cb629/ijms-19-00806-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/d3755c815013/ijms-19-00806-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/d1ceb0510f3d/ijms-19-00806-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/8ebcfa3b2d60/ijms-19-00806-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/c1f367dd6788/ijms-19-00806-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/72e722ef401c/ijms-19-00806-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/125c9af4da2e/ijms-19-00806-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/175610421b3d/ijms-19-00806-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/20dfe20a5312/ijms-19-00806-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/a1d2e32cb629/ijms-19-00806-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/d3755c815013/ijms-19-00806-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/d1ceb0510f3d/ijms-19-00806-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e025/5877667/8ebcfa3b2d60/ijms-19-00806-g009.jpg

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