The cytokinin response factors modulate root and shoot growth and promote leaf senescence in Arabidopsis

Abstract

SUMMARYThe cytokinin response factors (CRFs) are a group of related AP2/ERF transcription factors that are transcriptionally induced by cytokinin. Here we explore the role of the CRFs in Arabidopsis thaliana growth and development by analyzing lines with decreased and increased CRF function. While single crf mutations have no appreciable phenotypes, disruption of multiple CRFs results in larger rosettes, delayed leaf senescence, a smaller root apical meristem (RAM), reduced primary and lateral root growth, and, in etiolated seedlings, shorter hypocotyls. In contrast, overexpression of CRFs generally results in the opposite phenotypes. The crf1,2,5,6 quadruple mutant is embryo lethal, indicating that CRF function is essential for embryo development. Disruption of the CRFs results in partially insensitivity to cytokinin in a root elongation assay and affects the basal expression of a significant number of cytokinin-regulated genes, including the type-A ARRs, although it does not impair the cytokinin induction of the type-A ARRs. Genes encoding homeobox transcription factors are mis-expressed in the crf1,3,5,6 mutant, including STIMPY/WOX9 that is required for root and shoot apical meristem maintenance roots and which has previously been linked to cytokinin. These results indicate that the CRF transcription factors play important roles in multiple aspects of plant growth and development, in part through a complex interaction with cytokinin signaling.

CYTOKININ RESPONSE FACTOR2 (CRF2) and CRF3 Regulate Lateral Root Development in Response to Cold Stress in Arabidopsis

“…crf1,3,5,6 quadruple mutants displayed strong inhibition of primary root elongation compared with that of the wild type (Raines et al, 2016). LR numbers of both crf2,5,6 and crf3,5,6 triple mutants were reduced compared with the wild type (Raines et al, 2016).…”

“…Loss-offunction mutations in CRF2 or CRF3 or both CRF3 and CRF6 or CRF2, CRF3, and CRF6 caused reductions in root length, root meristem size, and LRP density, whereas overexpression of CRF2 or CRF3 or CRF6 enhanced LRP density ( Simá sková et al, 2015). In addition, multiple mutations in CRFs result in larger rosettes, delayed leaf senescence, and shorter hypocotyls in etiolated seedlings (Raines et al, 2016). These recent studies along with our present results indicate that the CRF genes play roles in regulating multiple aspects of plant growth and development including root system architecture and plant response to cold and freezing stress.…”

“…crf1,3,5,6 quadruple mutants displayed strong inhibition of primary root elongation compared with that of the wild type (Raines et al, 2016). LR numbers of both crf2,5,6 and crf3,5,6 triple mutants were reduced compared with the wild type (Raines et al, 2016). Loss-offunction mutations in CRF2 or CRF3 or both CRF3 and CRF6 or CRF2, CRF3, and CRF6 caused reductions in root length, root meristem size, and LRP density, whereas overexpression of CRF2 or CRF3 or CRF6 enhanced LRP density ( Simá sková et al, 2015).…”

Cytokinin response factors integrate auxin and cytokinin pathways for female reproductive organ development

“…Our understanding of the influence of auxin on the cell cycle is still fragmentary, but primary evidence indicates that auxin acts on several targets involved in the control of cell cycle (PerrotRechenmann, 2010). On the other hand, the ability of CKs to promote cell division, in particular through their action on D-type cyclins, was described several years ago (Dewitte et al, 2007;RiouKhamlichi et al, 1999), and it has been recently been shown that the transcript levels of several cell cycle-related genes were decreased in roots of the crf1,3,5,6 quadruple mutant (Raines et al, 2016).…”

The Hevea brasiliensis AP2/ERF superfamily: from ethylene signalling to latex harvesting and physiological disease response

“…Posttranslational modification was necessary to activate this phosphorylation site (Dubouzet et al, 2003;Liu et al, 1998). Phosphorylation regulation via histidine kinases has also been suggested for the ERF-VI (Raines et al, 2016). Another ERF belonging to the subgroup of ERF-IXb, AtERF104 required an interaction with the mitogen-activated protein kinase 6 (MPK6) for its stability (Bethke et al, 2009).…”