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<p>In this study, we evaluated the in vivo activity of the E1 element within the insulin promoter region. While we successfully obtained mice carrying a deletion exclusively in the E1 element of <i>Ins2</i> (2E mice), we were unable to obtain mice with a deletion limited to the E1 element of <i>Ins1</i>. To assess the role of the E1 element in <i>Ins1</i>, we compared the mice carrying deletions in the GG2-GG1/A2-C1 elements with or without an additional E1 element deletion (1GC/1GCE mice). 1GCE2E mice developed diabetes. In contrast, 1GCE2<sub>3</sub> mice (without deletion in the E1 element of <i>Ins2</i>) did not develop diabetes, suggesting that the E1 element of <i>Ins2</i> is critical for transcriptional regulation. Furthermore, 1GC2E mice (presence of the E1 element of <i>Ins1</i>) developed diabetes. However, the severity of the disease was milder in 1GC2E mice than in 1GCE2E mice, indicating that the E1 element of <i>Ins1</i> also contributes to transcriptional regulation. These data suggest that the E1 elements in both <i>Ins1/2</i> promoters are regulated for the in vivo transcription of insulin genes in mice.</p>

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In vivo activities of E1 elements in the insulin promoter

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月18日

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  • Hirofumi Noguchi,
  • Chika Miyagi-Shiohira,
  • Takuya Sadahira,
  • Masami Watanabe,
  • Issei Saitoh

摘要

In this study, we evaluated the in vivo activity of the E1 element within the insulin promoter region. While we successfully obtained mice carrying a deletion exclusively in the E1 element of Ins2 (2E mice), we were unable to obtain mice with a deletion limited to the E1 element of Ins1. To assess the role of the E1 element in Ins1, we compared the mice carrying deletions in the GG2-GG1/A2-C1 elements with or without an additional E1 element deletion (1GC/1GCE mice). 1GCE2E mice developed diabetes. In contrast, 1GCE23 mice (without deletion in the E1 element of Ins2) did not develop diabetes, suggesting that the E1 element of Ins2 is critical for transcriptional regulation. Furthermore, 1GC2E mice (presence of the E1 element of Ins1) developed diabetes. However, the severity of the disease was milder in 1GC2E mice than in 1GCE2E mice, indicating that the E1 element of Ins1 also contributes to transcriptional regulation. These data suggest that the E1 elements in both Ins1/2 promoters are regulated for the in vivo transcription of insulin genes in mice.