| Summary: | <p>Abstract</p> <p>Background</p> <p>The <it>Arabidopsis </it>response regulator 22 (ARR22) is one of two members of a recently defined novel group of two-component system (TCS) elements. TCSs are stimulus perception and response modules of prokaryotic origin, which signal by a His-to-Asp phosphorelay mechanism. In plants, TCS regulators are involved in hormone response pathways, such as those for cytokinin and ethylene. While the functions of the other TCS elements in <it>Arabidopsis</it>, such as histidine kinases (AHKs), histidine-containing phosphotransfer proteins (AHPs) and A-type and B-type ARRs are becoming evident, the role of ARR22 is poorly understood.</p> <p>Results</p> <p>We present evidence that ARR22 is a preferentially cytoplasmic protein, exclusively expressed in the chalaza of developing seeds. ARR22 specifically interacts with AHP2, AHP3 and AHP5 in yeast and living plant cells. Two new loss-of-function alleles, <it>arr22-2 </it>and <it>arr22-3</it>, were isolated and characterized. With respect to their morphology and metabolite status, no significant difference in the developing seeds of the <it>arr22 </it>mutants was observed compared to wild type. The genetic complementation of the <it>arr22 </it>mutants with a genomic <it>ARR22 </it>fragment resulted in plants (<it>arr22</it>/<it>gARR22</it>) with a pleiotropic phenotype of different penetrance. This phenotype was not observed when the phosphorylatable Asp74 of ARR22 was changed to either a dominant-active Glu or a dominant-inactive Asn. The phenotype of the <it>arr22</it>/<it>gARR22 </it>plants was comparable to that of multiple <it>ahk</it>, <it>ahp </it>and <it>B-type arr </it>mutants.</p> <p>Conclusion</p> <p>Our results favor the model that ARR22 acts as a phospho-histidine phosphatase on specific AHPs in the cytoplasm of <it>Arabidopsis </it>chalaza cells. The lack of any aberrant morphological and metabolite phenotype in the seeds of the <it>arr22 </it>mutants indicates that ARR22 is probably primarily responsible for the fine tuning of specific branches of chalaza-based TCS signalling. Even when slightly mis-expressed, ARR22 interferes with hormone homeostasis in non-chalaza tissues. Our data indicate that the chromatin status might play a crucial role in maintaining the chalaza-restricted expression of <it>ARR22</it>.</p>
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