Amiel Aliza, Reish Orit, Gaber Elena, Masterman Ronit, Tohami Tally, Fejgin Moshe D
Genetic Institute, Meir General Hospital, Kfar Saba, Israel.
Isr Med Assoc J. 2002 Sep;4(9):702-5.
While most allelic pairs of DNA replicate synchronously during the S phase of the cell cycle, some genes normally replicate asynchronously, i.e., genes on the X chromosome and imprinted genes. The replication control mechanism is unknown but was shown to be impaired in malignancies and chromosomal trisomies where replication pattern becomes asynchronous.
To determine the level of asynchronization in replication timing of cells from patients with microdeleted genomes.
We applied monocolor fluorescent in situ hybridization with different probes on leukocytes from microdeleted genomes.
All samples derived from the microdeleted genomes showed significantly higher levels of an asynchronized pattern compared to normal individuals.
Even a "small" genetic imbalance (microdeletion) can interfere with gene replication and cell cycle progression, as previously shown in full trisomies.
虽然大多数DNA等位基因对在细胞周期的S期同步复制,但一些基因通常异步复制,即X染色体上的基因和印记基因。复制控制机制尚不清楚,但在恶性肿瘤和染色体三体中显示受损,其中复制模式变为异步。
确定微缺失基因组患者细胞复制时间的异步水平。
我们在微缺失基因组的白细胞上应用了不同探针的单色荧光原位杂交。
与正常个体相比,所有来自微缺失基因组的样本均显示出明显更高水平的异步模式。
即使是“小”的基因失衡(微缺失)也会干扰基因复制和细胞周期进程,正如之前在完全三体中所显示的那样。