组蛋白变体的掺入,核心组蛋白的不同旁系同源物,染色质会影响细胞中所有DNA模板化的过程,包括转录的调节。近年来,很多研究都集中在H2A上。Z,在所有真核生物中发现的进化保守的H2A变体。为了探讨H2A的功能保守性。Z组蛋白在真核进化过程中我们转化了h2a。具有三个人H2A的z缺陷植物。Z蛋白评估其拯救突变缺陷的能力。我们发现人类H2A。Z.1和H2A。Z.2.1完全补充h2a的表型异常。z植物尽管事实上拟南芥和人类H2A。ZN-末端尾部序列是相当不同的。相比之下,大脑特异性剪接变体H2A。Z.2.2在野生型植物中具有显性负效应。此外,H2A.Z.1几乎完全恢复正常的H2A。h2a中的Z染色质占有率。z植物和恢复超过84%的错误表达基因的转录水平。最后,我们的假设是拟南芥H2A的N端尾部。Z并不是至关重要的,因为它的发育功能得到了拟南芥HTA11的N末端截短在很大程度上挽救h2a缺陷的能力的支持。z突变体。
The incorporation of histone variants, distinct paralogs of core histones, into chromatin affects all DNA-templated processes in the cell, including the regulation of transcription. In recent years, much research has been focused on
H2A.Z, an evolutionarily conserved H2A variant found in all eukaryotes. In order to investigate the functional conservation of H2A.Z histones during eukaryotic evolution we transformed
h2a.z deficient plants with each of the three human
H2A.Z variants to assess their ability to rescue the mutant defects. We discovered that human
H2A.Z.1 and
H2A.Z.2.1 fully complement the phenotypic abnormalities of
h2a.z plants despite significant divergence in the N-terminal tail sequences of Arabidopsis and human H2A.Zs. In contrast, the brain-specific splice variant H2A.Z.2.2 has a dominant-negative effect in wild-type plants, mimicking an
H2A.Z deficiency phenotype. Furthermore,
H2A.Z.1 almost completely re-establishes normal
H2A.Z chromatin occupancy in
h2a.z plants and restores the expression of more than 84% of misexpressed genes. Finally, we used a series of N-terminal tail truncations of Arabidopsis HTA11 to reveal that the N-terminal tail of Arabidopsis H2A.Z is not necessary for normal plant development but does play an important role in mounting proper environmental stress responses.