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一条在动物中保守且与高锌稳态途径平行起作用的低锌稳态途径。

A pathway for low zinc homeostasis that is conserved in animals and acts in parallel to the pathway for high zinc homeostasis.

作者信息

Dietrich Nicholas, Schneider Daniel L, Kornfeld Kerry

机构信息

Department of Developmental Biology, Washington University School of Medicine, Saint Louis, MO 63110, USA.

出版信息

Nucleic Acids Res. 2017 Nov 16;45(20):11658-11672. doi: 10.1093/nar/gkx762.

DOI:10.1093/nar/gkx762
PMID:28977437
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5714235/
Abstract

The essential element zinc plays critical roles in biology. High zinc homeostasis mechanisms are beginning to be defined in animals, but low zinc homeostasis is poorly characterized. We investigated low zinc homeostasis in Caenorhabditis elegans because the genome encodes 14 evolutionarily conserved Zrt, Irt-like protein (ZIP) zinc transporter family members. Three C. elegans zipt genes were regulated in zinc-deficient conditions; these promoters contained an evolutionarily conserved motif that we named the low zinc activation (LZA) element that was both necessary and sufficient for activation of transcription in response to zinc deficiency. These results demonstrated that the LZA element is a critical part of the low zinc homeostasis pathway. Transcriptional regulation of the LZA element required the transcription factor ELT-2 and mediator complex member MDT-15. We investigated conservation in mammals by analyzing LZA element function in human cultured cells; the LZA element-mediated transcriptional activation in response to zinc deficiency in cells, suggesting a conserved pathway of low zinc homeostasis. We propose that the pathway for low zinc homeostasis, which includes the LZA element and ZIP transporters, acts in parallel to the pathway for high zinc homeostasis, which includes the HZA element, HIZR-1 transcription factor and cation diffusion facilitator transporters.

摘要

必需元素锌在生物学中发挥着关键作用。动物体内高锌稳态机制已开始得到明确，但低锌稳态的特征却鲜为人知。我们对线虫的低锌稳态进行了研究，因为其基因组编码了14个进化上保守的Zrt、Irt样蛋白（ZIP）锌转运蛋白家族成员。在缺锌条件下，三种线虫zipt基因受到调控；这些启动子包含一个进化上保守的基序，我们将其命名为低锌激活（LZA）元件，该元件对于响应锌缺乏激活转录既必要又充分。这些结果表明，LZA元件是低锌稳态途径的关键部分。LZA元件的转录调控需要转录因子ELT - 2和中介体复合物成员MDT - 15。我们通过分析LZA元件在人类培养细胞中的功能来研究其在哺乳动物中的保守性；LZA元件在细胞中响应锌缺乏介导转录激活，表明存在一条保守的低锌稳态途径。我们提出，低锌稳态途径，包括LZA元件和ZIP转运蛋白，与高锌稳态途径并行发挥作用，高锌稳态途径包括HZA元件、HIZR - 1转录因子和阳离子扩散促进剂转运蛋白。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/f801ecbc73a1/gkx762fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/28304ba0a43c/gkx762fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/6eea404e530d/gkx762fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/16c2a56d48c6/gkx762fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/f7dd400cd313/gkx762fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/c125b3e2dbef/gkx762fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/22fce17e537d/gkx762fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/f801ecbc73a1/gkx762fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/28304ba0a43c/gkx762fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/6eea404e530d/gkx762fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/16c2a56d48c6/gkx762fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/f7dd400cd313/gkx762fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/c125b3e2dbef/gkx762fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/22fce17e537d/gkx762fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a67/5714235/f801ecbc73a1/gkx762fig7.jpg

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