Liu Desheng, Makaroff Christopher A
BMC Plant Biol. 2015 Mar 5;15:74. doi: 10.1186/s12870-015-0452-2.
Eco1/Ctf7 is essential for the establishment of sister chromatid cohesion during S phase of the cell cycle. Inactivation of Ctf7/Eco1 leads to a lethal phenotype in most organisms. Altering Eco1/Ctf7 levels or point mutations in the gene can lead to alterations in nuclear division as well as a wide range of developmental defects. Inactivation of Arabidopsis CTF7 (AtCTF7) results in severe defects in reproduction and vegetative growth.
To further investigate the function(s) of AtCTF7, a tagged version of AtCTF7 and several AtCTF7 deletion constructs were created and transformed into wild type or ctf7 +/- plants. Transgenic plants expressing 35S:NTAP:AtCTF7∆299-345 (AtCTF7∆B) displayed a wide range of phenotypic alterations in reproduction and vegetative growth. Male meiocytes exhibited chromosome fragmentation and uneven chromosome segregation. Mutant ovules contained abnormal megasporocyte-like cells during pre-meiosis, megaspores experienced elongated meiosis and megagametogenesis, and defective megaspores/embryo sacs were produced at various stages. The transgenic plants also exhibited a broad range of vegetative defects, including meristem disruption and dwarfism that were inherited in a non-Mendelian fashion. Transcripts for epigenetically regulated transposable elements (TEs) were elevated in transgenic plants. Transgenic plants expressing 35S:AtCTF7∆B displayed similar vegetative defects, suggesting the defects in 35S:NTAP:AtCTF7∆B plants are caused by high-level expression of AtCTF7∆B.
High level expression of AtCTF7∆B disrupts megasporogenesis, megagametogenesis and male meiosis, as well as causing a broad range of vegetative defects, including dwarfism that are inherited in a non-Mendelian fashion.
Eco1/Ctf7对于细胞周期S期姐妹染色单体黏连的建立至关重要。在大多数生物体中，Ctf7/Eco1的失活会导致致死表型。改变Eco1/Ctf7的水平或该基因中的点突变会导致核分裂改变以及广泛的发育缺陷。拟南芥CTF7（AtCTF7）的失活会导致生殖和营养生长方面的严重缺陷。
为了进一步研究AtCTF7的功能，构建了AtCTF7的标签版本和几个AtCTF7缺失构建体，并将其转化到野生型或ctf7+/-植物中。表达35S:NTAP:AtCTF7∆299 - 345（AtCTF7∆B）的转基因植物在生殖和营养生长方面表现出广泛的表型改变。雄配子体细胞表现出染色体片段化和染色体分离不均。突变胚珠在减数分裂前含有异常的大孢子母细胞样细胞，大孢子经历延长的减数分裂和雌配子体发育，并且在各个阶段产生有缺陷的大孢子/胚囊。转基因植物还表现出广泛的营养缺陷，包括分生组织破坏和侏儒症，这些缺陷以非孟德尔方式遗传。表观遗传调控的转座元件（TEs）的转录本在转基因植物中升高。表达35S:AtCTF7∆B的转基因植物表现出类似的营养缺陷，表明35S:NTAP:AtCTF7∆B植物中的缺陷是由AtCTF7∆B的高水平表达引起的。
AtCTF7∆B的高水平表达破坏了大孢子发生、雌配子体发育和雄配子体减数分裂，以及导致广泛的营养缺陷，包括以非孟德尔方式遗传的侏儒症。
