DIFFERENTIAL TRANSCRIPTION OF PGK GENES DURING SPERMATOGENESIS IN THE MOUSE
DIFFERENTIAL TRANSCRIPTION OF PGK GENES DURING SPERMATOGENESIS IN THE MOUSE
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DOI：
10.1016/0012-1606(92)90056-m
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发表时间：
1992-11-01
影响因子：
2.7
通讯作者：
ROSSI, JJ
中科院分区：
文献类型：
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作者：
MCCARREY, JR;BERG, WM;ROSSI, JJ
我们分析了小鼠精子发生过程中普遍表达的x -linked pgk -1基因和睾丸特异性的autosomalpgk -2基因产生的转录本的发生情况。我们发现这些mrna的组织特异性、发育特异性和细胞类型特异性与先前报道的磷酸甘油酸激酶（PGK）的两种蛋白同工酶相似。这表明，在精子发生过程中，pgk基因差异表达的主要调控是在转录水平上发挥作用的。我们首先在瘦前期精母细胞中检测到pgk - 2mrna，表明pgk -2的转录在男性生殖细胞减数分裂开始时启动，然后在后期精母细胞和减数分裂后圆形精母细胞中继续增加。这种表达在粗线精母细胞中观察到的pgk -1转录物水平最初下降之前开始，这显然是在生精细胞中单个X染色体失活之后发生的。然而，与雌性体细胞中失活的X染色体停止pgk -1转录不同，我们发现生精细胞中pgk -1位点失活后，启动子区域的关键CpG二核苷酸不会甲基化。这些结果支持了pgk -2基因在减数分裂和减数分裂后生精细胞中的特异性表达，以补偿这些细胞中由短暂的x染色体失活引起的pgk -1基因产物水平的降低。他们进一步表明，受精后不久父本pgk -1等位基因的转录重新启动是由精子发生过程中该基因启动子区域的组成性低甲基化促进的。
We have analyzed the occurrence of transcripts produced from the ubiquitously expressed, X-linkedPgk-1gene and the testis-specific, autosomalPgk-2gene during spermatogenesis in the mouse. We found that tissue specificity, developmental specificity, and cell-type specificity of these mRNAs parallel that previously reported for the two protein isozymes of phosphoglycerate kinase (PGK) encoded by these two genes. This indicates that primary regulation of differential expression of thePgkgenes during spermatogenesis is exerted at the transcriptional level. We first detectedPgk-2mRNA in preleptotene spermatocytes, indicating that transcription ofPgk-2is initiated coincident with the onset of meiosis in male germ cells, and then continues to increase in later spermatocytes and postmeiotic round spermatids. This expression initiates prior to an initial decline inPgk-1transcript levels observed in pachytene spermatocytes, which apparently follows inactivation of the single X chromosome in spermatogenic cells. However, unlike cessation ofPgk-1transcription from the inactivated X chromosome in female somatic cells, we show that inactivation of thePgk-1locus in spermatogenic cells is not followed by methylation of a key CpG dinucleotide in the promoter region. These results support the idea that specific expression of thePgk-2gene in meiotic and postmeiotic spermatogenic cells has evolved to compensate for reduced levels ofPgk-1gene product caused by transient X-chromosome inactivation in these cells. They further suggest that reinitiation of transcription of the paternalPgk-1allele shortly after fertilization is facilitated by constitutive hypomethylation in the promoter region of this gene throughout spermatogenesis.