•　Background　and　Aims　INDETERMINATE　DOMAIN　10　(IDD10)　is　a　key　transcription　factor　gene　that　activates　the　expression　of　a　large　number　of　NH4+-responsive　genes　including　AMMONIUM　TRANSPORTER　1;2　(AMT1;2).　Primary　root　growth　of　rice　(Oryza　sativa)　idd10　mutants　is　hypersensitive　to　NH4+.　The　involvement　of　CALCINEURIN　B-LIKE　INTERACTING　PROTEIN　KINASE　(CIPK)　genes　in　the　action　of　IDD10　on　NH4+-　mediated　root　growth　was　investigated.　•　Methods　Quantitative　reverse　transcription–PCR　was　used　to　analyse　NH4+-　and　IDD10-dependent　expression　of　CIPK　genes.　IDD10-regulated　CIPK　target　genes　were　identified　using　electrophoretic　mobility　shift　assays,　chromatin　immunoprecipitation　and　transient　transcription　assays.　Root　growth　rate,　ammonium　content　and　15N　uptake　of　cipk　mutants　were　measured　to　determine　their　sensitivity　to　NH4+　and　to　compare　these　phenotypes　with　those　of　idd10.　The　genetic　relationship　between　CIPK9　OX　and　idd10　was　investigated　by　crosses　between　the　CIPK9　and　IDD10　lines.　•　Key　Results　AMT1;2　was　overexpressed　in　idd10　to　determine　whether　NH4+-hypersensitive　root　growth　of　idd10　resulted　from　limitations　in　NH4+　uptake　or　from　low　cellular　levels　of　NH4+.　High　NH4+　levels　in　idd10/　AMT1;2　OX　did　not　rescue　the　root　growth　defect.　Next,　the　involvement　of　CIPK　genes　in　NH4+-dependent　root　growth　and　interactions　between　IDD10　and　CIPK　genes　was　investigated.　Molecular　analysis　revealed　that　IDD10　directly　activated　transcription　of　CIPK9　and　CIPK14.　Expression　of　CIPK8,　9,　14/15　and　23　was　sensitive　to　exogenous　NH4+.　Further　studies　revealed　that　cipk9　and　idd10　had　almost　identical　NH4+-sensitive　root　phenotypes,　including　low　efficiency　of　15NH4+　uptake.　Analysis　of　plants　containing　both　idd10　and　CIPK9　OX　showed　that　CIPK9　OX　could　rescue　the　NH4+-dependent　root　growth　defects　of　idd10.　•　Conclusions　CIPK9　was　involved　in　NH4+-dependent　root　growth　and　appeared　to　act　downstream　of　IDD10.　This　information　will　be　useful　in　future　explorations　of　NH4+　signalling　in　plants.　©　The　Author(s)　2019.　Published　by　Oxford　University　Press　on　behalf　of　the　Annals　of　Botany　Company.　All　rights　reserved.