Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 Aug 30;45(20):11658–11672. doi: 10.1093/nar/gkx762

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2017. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

PMC Copyright notice

Figure 7. — Models of transcriptional regulation during zinc deficiency. (A) Diagram of an intestinal cell flanked by the intestinal lumen (above) and the pseudocoelom (below). Two dietary zinc-conditions are illustrated: deficiency (left) and excess (right). Zinc (black circles) enters the intestinal cell, and an undefined sensing mechanism causes activation of LZA element containing promoters. ZIPT proteins (blue) might localize to the plasma membrane or lysosome related organelles (LRO, green), but the subcellular localization has not been established. During zinc excess, the HIZR-1 nuclear receptor causes activation of HZA element containing promoters and the CDF-2 protein (red) localizes to the LRO where it functions to store zinc, and the TTM-1B protein (red) localizes to the plasma membrane where it functions to excrete zinc. (B) Two models of LZA element mediated transcriptional regulation. In the upper model, a proposed LZA element binding protein (blue box) is a transcriptional activator that interacts with the LZA element in response to zinc deficiency; this triggers assembly of a transcriptional activation complex including MDT-15 (green box). ELT-2 (yellow box) constitutively binds GATA elements and is permissive for intestinal cell expression. Stimulation is shown by an arrow and thick transcription start site. In the lower model, the LZA-element binding protein is a transcriptional repressor that interacts with the LZA element during zinc-replete conditions. Repression is shown by a bar and thin transcription start site; zinc deficiency abrogates the binding interaction, allowing assembly of a transcriptional activation complex. These two models are not mutually exclusive, since the LZA element binding protein might be converted from a repressor in zinc-replete conditions to an activator in zinc-deficient conditions.