AUTHOR=Sun Tong , Wang Ting , Qiang Yalin , Zhao Gangqing , Yang Jian , Zhong Hua , Peng Xiaojue , Yang Jing , Li Yangsheng 

TITLE=CBL-Interacting Protein Kinase OsCIPK18 Regulates the Response of Ammonium Toxicity in Rice Roots

JOURNAL=Frontiers in Plant Science

VOLUME=13

YEAR=2022

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2022.863283

DOI=10.3389/fpls.2022.863283

ISSN=1664-462X

ABSTRACT=<p>Ammonium (<inline-formula><mml:math id="M1" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msubsup><mml:mrow><mml:mtext>NH</mml:mtext></mml:mrow><mml:mrow><mml:mn>4</mml:mn></mml:mrow><mml:mrow><mml:mo>+</mml:mo></mml:mrow></mml:msubsup></mml:math></inline-formula>) is one of the major nitrogen sources for plants. However, excessive ammonium can cause serious harm to the growth and development of plants, i.e., ammonium toxicity. The primary regulatory mechanisms behind ammonium toxicity are still poorly characterized. In this study, we showed that OsCIPK18, a CBL-interacting protein kinase, plays an important role in response to ammonium toxicity by comparative analysis of the physiological and whole transcriptome of the T-DNA insertion mutant (<italic>cipk18</italic>) and the wild-type (WT). Root biomass and length of <italic>cipk18</italic> are less inhibited by excess <inline-formula><mml:math id="M2" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msubsup><mml:mrow><mml:mtext>NH</mml:mtext></mml:mrow><mml:mrow><mml:mn>4</mml:mn></mml:mrow><mml:mrow><mml:mo>+</mml:mo></mml:mrow></mml:msubsup></mml:math></inline-formula> compared with WT, indicating increased resistance to ammonium toxicity. Transcriptome analysis reveals that OsCIPK18 affects the <inline-formula><mml:math id="M3" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msubsup><mml:mrow><mml:mtext>NH</mml:mtext></mml:mrow><mml:mrow><mml:mn>4</mml:mn></mml:mrow><mml:mrow><mml:mo>+</mml:mo></mml:mrow></mml:msubsup></mml:math></inline-formula> uptake by regulating the expression of OsAMT1;2 and other <inline-formula><mml:math id="M4" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msubsup><mml:mrow><mml:mtext>NH</mml:mtext></mml:mrow><mml:mrow><mml:mn>4</mml:mn></mml:mrow><mml:mrow><mml:mo>+</mml:mo></mml:mrow></mml:msubsup></mml:math></inline-formula> transporters, but does not affect ammonium assimilation. Differentially expressed genes induced by excess <inline-formula><mml:math id="M5" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msubsup><mml:mrow><mml:mtext>NH</mml:mtext></mml:mrow><mml:mrow><mml:mn>4</mml:mn></mml:mrow><mml:mrow><mml:mo>+</mml:mo></mml:mrow></mml:msubsup></mml:math></inline-formula> in WT and <italic>cipk18</italic> were associated with functions, such as ion transport, metabolism, cell wall formation, and phytohormones signaling, suggesting a fundamental role for OsCIPK18 in ammonium toxicity. We further identified a transcriptional regulatory network downstream of OsCIPK18 under <inline-formula><mml:math id="M6" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msubsup><mml:mrow><mml:mtext>NH</mml:mtext></mml:mrow><mml:mrow><mml:mn>4</mml:mn></mml:mrow><mml:mrow><mml:mo>+</mml:mo></mml:mrow></mml:msubsup></mml:math></inline-formula> stress that is centered on several core transcription factors. Moreover, OsCIPK18 might function as a transmitter in the auxin and abscisic acid (ABA) signaling pathways affected by excess ammonium. These data allowed us to define an OsCIPK18-regulated/dependent transcriptomic network for the response of ammonium toxicity and provide new insights into the mechanisms underlying ammonium toxicity.</p>