Kato K, Kanamori A, Kondoh H
Department of Molecular Biology, School of Science, Nagoya University, Japan.
Mol Cell Biol. 1990 Feb;10(2):486-91. doi: 10.1128/mcb.10.2.486-491.1990.
The level of expression of N-myc in mouse teratocarcinoma stem cells is very high. Previous studies have shown that N-myc expression significantly decreases when the stem cells are subjected to long-term induction for differentiation by retinoic acid (RA). We found that in a stem cell line, OTF9, a steep yet transient decrease of N-myc expression takes place much earlier, immediately after induction by RA. To examine whether this decrease is responsible for differentiation, we constructed a gene, miwNmyc, to express N-myc cDNA constitutively and transformed OTF9 cells with this gene construct. Transformants under the constitutive expression of miwNmyc differentiated normally, as judged by morphological changes and by modulation of c-myc, Hox1.1, and laminin B1 expression. Therefore, transient decrease of N-myc expression may be the consequence of RA-induced differentiation, even though it occurs very early in the process. Alternatively, in addition to N-myc decrease, there may be redundant mechanisms which lead to OTF9 differentiation after induction by RA, so that suppression of N-myc decrease is bypassed by at least one other mechanism.
N - myc在小鼠畸胎瘤干细胞中的表达水平非常高。先前的研究表明，当干细胞受到视黄酸（RA）长期诱导分化时，N - myc的表达会显著降低。我们发现，在一个干细胞系OTF9中，N - myc表达会在RA诱导后立即出现急剧但短暂的下降，且发生时间要早得多。为了研究这种下降是否与分化有关，我们构建了一个基因miwNmyc，用于组成性表达N - myc cDNA，并将该基因构建体转染到OTF9细胞中。根据形态变化以及c - myc、Hox1.1和层粘连蛋白B1表达的调节情况判断，在miwNmyc组成性表达下的转化细胞能够正常分化。因此，N - myc表达的短暂下降可能是RA诱导分化的结果，尽管它在这个过程中很早就出现了。或者，除了N - myc的下降之外，可能还存在冗余机制，这些机制在RA诱导后导致OTF9分化，从而使得至少一种其他机制绕过了对N - myc下降的抑制。
