Barber Michael C, Vallance Amanda J, Kennedy Helen T, Travers Maureen T
Hannah Research Institute, Ayr KA6 5HL, Scotland, UK.
Biochem J. 2003 Oct 15;375(Pt 2):489-501. doi: 10.1042/BJ20030480.
ACC-alpha (acetyl-CoA carboxylase-alpha), a key regulator of fatty-acid metabolism, is encoded by mRNAs transcribed from three promoters, PI, PII and PIII, in the ovine genome. Enhanced expression of transcripts encoded by PIII in mammary gland during lactation is associated with alterations in chromatin structure that result in the detection of two DNase I hypersensitive sites, upstream of the start site. The most proximal site, located between -190 and -10, is characterized by the presence of an inverted-CCAAT box, C2 at -167, and E-boxes, E1 and E2, at -151 and -46. Deletion of these motifs, which bind nuclear factor-Y and upstream stimulatory factors respectively in gel-shift assays, attenuates the activity of luciferase reporter constructs in transfected cells. Chromatin immunoprecipitation demonstrated that these transcription factors were associated with PIII in vivo in both lactating and non-lactating mammary tissues. The basic helix-loop-helix-leucine zipper transcription factor, SREBP-1 (sterol-regulated-element-binding protein-1), transactivated PIII reporter constructs in transfected HC11 mammary cells, and this was dependent on the presence of E1, but not on C2 or E2. SREBP-1 was only associated with PIII in chromatin from lactating animals, which was coincident with a 4-fold increase in the precursor (125 kDa) form of SREBP-1 in microsomes and the appearance of the mature form (68 kDa) in the nucleus. SREBP-1 motifs are also present in the proximal region of PII, which is also induced in lactation. This indicates that SREBP-1 is a major developmental regulator of the programme of lipid synthesis de novo in the lactating mammary gland.
乙酰辅酶A羧化酶α(ACC-α)是脂肪酸代谢的关键调节因子,由绵羊基因组中从PI、PII和PIII三个启动子转录的mRNA编码。泌乳期间乳腺中由PIII编码的转录本表达增强,与染色质结构改变有关,这种改变导致在起始位点上游检测到两个脱氧核糖核酸酶I超敏位点。最靠近近端的位点位于-190至-10之间,其特征是存在一个反向CCAAT框(位于-167处的C2)以及位于-151和-46处的E框(E1和E2)。在凝胶迁移试验中,这些分别与核因子-Y和上游刺激因子结合的基序缺失,会减弱荧光素酶报告基因构建体在转染细胞中的活性。染色质免疫沉淀表明,这些转录因子在泌乳和非泌乳乳腺组织中均在体内与PIII相关。碱性螺旋-环-螺旋-亮氨酸拉链转录因子固醇调节元件结合蛋白-1(SREBP-1)在转染的HC11乳腺细胞中反式激活PIII报告基因构建体,这依赖于E1的存在,但不依赖于C2或E2。SREBP-1仅在泌乳动物的染色质中与PIII相关,这与微粒体中SREBP-1前体(125 kDa)形式增加4倍以及细胞核中成熟形式(68 kDa)的出现相一致。SREBP-1基序也存在于PII的近端区域,PII在泌乳期也被诱导。这表明SREBP-1是泌乳期乳腺中从头合成脂质程序的主要发育调节因子。