AUTHOR=Hermann Meike , Maier Felix , Masroor Ashir , Hirth Sofia , Pfitzner Artur J., Pfitzner Ursula M.

TITLE=The Arabidopsis NIMIN proteins affect NPR1 differentially

JOURNAL=Frontiers in Plant Science

VOLUME=4

YEAR=2013

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2013.00088

DOI=10.3389/fpls.2013.00088

ISSN=1664-462X

ABSTRACT=<p>NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) is the central regulator of the pathogen defense reaction systemic acquired resistance (SAR). NPR1 acts by sensing the SAR signal molecule salicylic acid (SA) to induce expression of <italic>PATHOGENESIS-RELATED</italic> (<italic>PR</italic>) genes. Mechanistically, NPR1 is the core of a transcription complex interacting with TGA transcription factors and NIM1-INTERACTING (NIMIN) proteins. <italic>Arabidopsis</italic> NIMIN1 has been shown to suppress NPR1 activity in transgenic plants. The <italic>Arabidopsis</italic><italic>NIMIN</italic> family comprises four structurally related, yet distinct members. Here, we show that <italic>NIMIN1</italic>, <italic>NIMIN2</italic>, and <italic>NIMIN3</italic> are expressed differentially, and that the encoded proteins affect expression of the SAR marker <italic>PR-1</italic> differentially. <italic>NIMIN3</italic> is expressed constitutively at a low level, but <italic>NIMIN2</italic> and <italic>NIMIN1</italic> are both responsive to SA. While <italic>NIMIN2</italic> is an immediate early SA-induced and <italic>NPR1</italic>-independent gene, <italic>NIMIN1</italic> is activated after <italic>NIMIN2</italic>, but clearly before <italic>PR-1</italic>. Notably, <italic>NIMIN1</italic>, like <italic>PR-1</italic>, depends on <italic>NPR1</italic>. In a transient assay system, NIMIN3 suppresses SA-induced <italic>PR-1</italic> expression, albeit to a lesser extent than NIMIN1, whereas NIMIN2 does not negatively affect <italic>PR-1</italic> gene activation. Furthermore, although binding to the same domain in the C-terminus, NIMIN1 and NIMIN2 interact differentially with NPR1, thus providing a molecular basis for their opposing effects on NPR1. Together, our data suggest that the <italic>Arabidopsis</italic> NIMIN proteins are regulators of the SAR response. We propose that NIMINs act in a strictly consecutive and SA-regulated manner on the SA sensor protein NPR1, enabling NPR1 to monitor progressing threat by pathogens and to promote appropriate defense gene activation at distinct stages of SAR. In this scenario, the defense gene <italic>PR-1</italic> is repressed at the onset of SAR by SA-induced, yet instable NIMIN1.</p>