<p>According to our study and previous reports [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005399#pgen.1005399.ref027" target="_blank">27</a>,<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005399#pgen.1005399.ref031" target="_blank">31</a>], we propose a coherent feed-forward loop that involves EIN3 and ORE1 in regulating ethylene-mediated chl degradation. EIN3 directly represses the transcription of <i>miR164</i>, which negatively regulates <i>ORE1</i> at the post-transcriptional level. Meanwhile, EIN3 can directly bind to the <i>ORE1</i> promoter and induce <i>ORE1</i> transcription. Three <i>CCGs</i>, <i>NYE1</i>, <i>NYC1</i>, and <i>PAO</i>, are the direct targets of EIN3. As a transcription factor downstream of EIN3, ORE1 shares these 3 common direct targets with EIN3. However, ORE1 also has its own distinct target, <i>NOL</i>, during the regulation of chl degradation. The broad range of expression of <i>CCGs</i> leads to chl degradation, the early step of leaf senescence. In addition, ORE1 directly activates the expression of <i>ACS2</i>, which presumably triggers a positive feedback regulation of ethylene synthesis. Arrows and bars represent positive and negative regulations, respectively.</p
