RESUMO
The transit from indeterminate to determinate root developmental program compromises growth and causes the differentiation of the meristem, but a direct link between this process with auxin signaling and/or viability of initial cells remains untested. Here, through the isolation and characterization of the halted primary root1 (hpr1) mutant of Arabidopsis, which develops primary and lateral roots with genetically stable determinate growth after germination, we show that the differentiation of the root meristem correlates with enhanced auxin responsiveness and is preceded by the death of provasculature initial cells in both primary and lateral roots. Supplementation of indole-3-acetic acid causes both a dose-dependent repression of primary root growth and an induction of DR5:uidA expression in wild-type seedlings, and these effects were exacerbated in hpr1 mutants. The damage of provasculature initial cells in the root of hpr1 mutants occurred at earlier times than the full differentiation of the meristem, and correlates with a reduced expression domain of CycB1:uidA and PRZ:uidA. Thus, HPR1 plays critical functions for stem cell maintenance, auxin homeostasis, cell division in the meristem, and indeterminate root growth.
Assuntos
Proteínas de Arabidopsis/química , Ácidos Indolacéticos/metabolismo , Raízes de Plantas/químicaRESUMO
Roots have both indeterminate and determinate developmental programs. The latter is preceded by the former. It is not well understood how the indeterminacy-to-determinacy switch (IDS) is regulated. We isolated a moots koom2 (mko2; 'short root' in Mayan) Arabidopsis thaliana mutant with determinate primary root growth and analyzed the root apical meristem (RAM) behavior using various marker lines. Deep sequencing and genetic and pharmacological complementation permitted the identification of a point mutation in the FOLYLPOLYGLUTAMATE SYNTHETASE1 (FPGS1) gene responsible for the mko2 phenotype. Wild-type FPGS1 is required to maintain the IDS in the 'off' state. When FPGS1 function is compromised, the IDS is turned on and the RAM becomes completely consumed. The polyglutamate-dependent pathway of the IDS involves activation of the quiescent center independently of auxin gradients and regulatory modules participating in RAM maintenance (WUSCHEL-RELATED HOMEOBOX5 (WOX5), PLETHORA, and SCARECROW (SCR)). The mko2 mutation causes drastic changes in folate metabolism and also affects lateral root primordium morphogenesis but not initiation. We identified a metabolism-dependent pathway involved in the IDS in roots. We suggest that the root IDS represents a specific developmental pathway that regulates RAM behaviour and is a different level of regulation in addition to RAM maintenance.