Cyclin‐dependent kinase‐activating kinases <scp>CDKD</scp>;1 and <scp>CDKD</scp>;3 are essential for preserving mitotic activity in <i>Arabidopsis thaliana</i>

<jats:title>Summary</jats:title><jats:p>For the full activation of cyclin‐dependent kinases (<jats:styled-content style="fixed-case">CDK</jats:styled-content>s), not only cyclin binding but also <jats:styled-content style="fixed-case">CDK</jats:styled-content> phosphorylation is required. This activating phosphorylation is mediated by <jats:styled-content style="fixed-case">CDK</jats:styled-content>‐activating kinases (<jats:styled-content style="fixed-case">CAK</jats:styled-content>s). Arabidopsis has four genes showing similarity to vertebrate‐type <jats:styled-content style="fixed-case">CAK</jats:styled-content>s, three <jats:italic><jats:styled-content style="fixed-case">CDKD</jats:styled-content></jats:italic>s (<jats:italic><jats:styled-content style="fixed-case">CDKD</jats:styled-content>;1</jats:italic>‐<jats:italic><jats:styled-content style="fixed-case">CDKD</jats:styled-content>;3</jats:italic>) and one <jats:italic><jats:styled-content style="fixed-case">CDKF</jats:styled-content></jats:italic> (<jats:italic><jats:styled-content style="fixed-case">CDKF</jats:styled-content>;1</jats:italic>). We previously found that the <jats:italic>cdkf;1</jats:italic> mutant is defective in post‐embryonic development, even though the kinase activities of core <jats:styled-content style="fixed-case">CDK</jats:styled-content>s remain unchanged relative to the wild type. This raised a question about the involvement of <jats:styled-content style="fixed-case">CDKD</jats:styled-content>s in <jats:styled-content style="fixed-case">CDK</jats:styled-content> activation <jats:italic>in planta</jats:italic>. Here we report that the <jats:italic>cdkd;1 cdkd;3</jats:italic> double mutant showed gametophytic lethality. Most <jats:italic>cdkd;1‐1 cdkd;3‐1</jats:italic> pollen grains were defective in pollen mitosis I and <jats:styled-content style="fixed-case">II</jats:styled-content>, producing one‐cell or two‐cell pollen grains that lacked fertilization ability. We also found that the double knock‐out of <jats:italic><jats:styled-content style="fixed-case">CDKD</jats:styled-content>;1</jats:italic> and <jats:italic><jats:styled-content style="fixed-case">CDKD</jats:styled-content>;3</jats:italic> caused arrest and/or delay in the progression of female gametogenesis at multiple steps. Our genetic analyses revealed that the functions of <jats:styled-content style="fixed-case">CDKF</jats:styled-content>;1 and <jats:styled-content style="fixed-case">CDKD</jats:styled-content>;1 or <jats:styled-content style="fixed-case">CDKD</jats:styled-content>;3 do not overlap, either during gametophyte and embryo development or in post‐embryonic development. Consistent with these analyses, <jats:italic><jats:styled-content style="fixed-case">CDKF</jats:styled-content>;1</jats:italic> expression in the <jats:italic>cdkd;1‐1 cdkd;3‐1</jats:italic> mutant could not rescue the gametophytic lethality. These results suggest that, in Arabidopsis, <jats:styled-content style="fixed-case">CDKD</jats:styled-content>;1 and <jats:styled-content style="fixed-case">CDKD</jats:styled-content>;3 function as <jats:styled-content style="fixed-case">CAK</jats:styled-content>s controlling mitosis, whereas <jats:styled-content style="fixed-case">CDKF</jats:styled-content>;1 plays a distinct role, mainly in post‐embryonic development. We propose that <jats:styled-content style="fixed-case">CDKD</jats:styled-content>;1 and <jats:styled-content style="fixed-case">CDKD</jats:styled-content>;3 phosphorylate and activate all core <jats:styled-content style="fixed-case">CDK</jats:styled-content>s, <jats:styled-content style="fixed-case">CDKA</jats:styled-content>,<jats:styled-content style="fixed-case"> CDKB</jats:styled-content>1 and <jats:styled-content style="fixed-case">CDKB</jats:styled-content>2, thereby governing cell cycle progression throughout plant development.</jats:p>