The GATA-factor elt-2 is essential for formation of the Caenorhabditis elegans intestine
The GATA-factor elt-2 is essential for formation of the Caenorhabditis elegans intestine
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DOI：
10.1016/s0012-1606(98)80006-7
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发表时间：
1998-06-15
影响因子：
2.7
通讯作者：
McGhee, JD
中科院分区：
文献类型：
--
作者：
Fukushige, T;Hawkins, MG;McGhee, JD
秀丽隐杆线虫的elt - 2基因编码一种单指GATA因子，先前因其与控制肠道特异性ges - 1酯酶基因的一对串联GATA位点结合而被克隆。在本文中，我们表明elt - 2的表达完全是肠道特异性的，从胚胎肠道只有两个细胞时开始（在ges - 1表达之前的一个细胞周期），并在蠕虫的整个生命周期中在肠道的每个细胞中持续表达。当使用转基因热激构建体异位表达elt - 2时，内源性ges - 1基因现在在胚胎的大多数（如果不是全部）细胞中表达；在同一实验中，其他几种肠道标记物（包括一个用于检测elt - 2自身调节的转基因elt - 2启动子:: lacZ报告基因构建体）也异位表达。这些效应是特异性的，因为另外两种秀丽隐杆线虫GATA因子（elt - 1和elt - 3）不会导致肠道基因异位表达。鉴定出一种不精确的转座子切除，它去除了整个elt - 2编码区。纯合的elt - 2缺失突变体在L1幼虫阶段死亡，肠道细胞明显畸形或退化。尽管elt - 2功能的丧失对后期肠道形态发生和功能有重大影响，但突变胚胎仍然表达ges - 1。我们认为elt - 2是控制胚胎肠道发育的一个冗余基因网络的一部分；其他因子可能能够在肠道发育的早期阶段补偿elt - 2的缺失，但在后期阶段则不能。我们讨论了这个调控网络的元件是否在所有后生动物中都保守。（C）1998学术出版社
The Caenorhabditis elegans elt-2 gene encodes a single-finger GATA factor, previously cloned by virtue of its binding to a tandem pair of GATA sites that control the gut-specific ges-l esterase gene. In the present paper, we show that elt-2 expression is completely gut specific, beginning when the embryonic gut has only two cells (one cell cycle prior to ges-l expression) and continuing in every cell of the gut throughout the life of the worm. When elt-2 is expressed ectopically using a transgenic heat-shock construct, the endogenous ges-l gene is now expressed in most if not all cells of the embryo; several other gut markers (including a transgenic elt-2-promoter::lacZ reporter construct designed to test for elt-2 autoregulation) are also expressed ectopically in the same experiment. These effects are specific in that two other C. elegans GATA factors (elt-1 and elt-3) do not cause ectopic gut gene expression. An imprecise transposon excision was identified that removes the entire elt-2 coding region. Homozygous elt-2 null mutants die at the L1 larval stage with an apparent malformation or degeneration of gut cells. Although the loss of elt-2 function has major consequences for later gut morphogenesis and function, mutant embryos still express ges-1. We suggest that elt-2 is part of a redundant network of genes that controls embryonic gut development; other factors may be able to compensate for elt-2 loss in the earlier stages of gut development but not in later stages. We discuss whether elements of this regulatory network may be conserved in all metazoa. (C) 1998 Academic Press.