RML1 and RML2, Arabidopsis Genes Required for Cell Proliferation at the Root Tip

Abstract

New cells are produced from the meristematic tissues located at the shoot and root tip throughout the life of higher plants. To investigate the genetic mechanism regulating meristematic activity, we isolated and characterized four single-gene, recessive mutants in Arabidopsis fhaliana called root meristemless (rmn. Complementation tests identified two RML loci; RML7 maps to chromosome IV and RML2 maps to chromosome 111. These mutants produce normal embryonic roots that either did not undergo or experienced limited cell division following germination, resulting in primary roots of less than 2.0 mm in length. Mutants can produce lateral and adventitious roots, which can grow to a length comparable to the embryonic root and arrest, indicating that the growth arrest is unrelated to the embryonic dormancy process. Neither the addition of growth regulators to the media nor the removal of shoots can rescue mutant roots from growth arrest, indicating that the mutant phenotype is not caused by a shortage of known growth regulators or by a transmissible shoot inhibitor. Normal cell division ability in mutant embryo, shoot, and callus cells indicates that the RML gene functions are not part of the general cell division processes; rather, they are involved specifically in activating the cell division cycle in the root apical cells.The sporophytic phase of seed plants consists of embryonic and postembryonic development (Esau, 1977). Following fertilization, the zygote undergoes rapid cell division to produce the embryo. In accordance with the developmental program, the embryo ceases cell proliferation upon maturation and then enters dormancy. Postembryonic development begins with imbibition and germination; cell division is activated in the shoot and root apical cells, generating the shoot and root meristems (Steeves and Sussex, 1989). These apical meristematic cells can remain in the cell cycle to generate new cells for growth and development throughout the plant's life (Lyndon, 1990). Behind the apical meristems, the cell division rate decreases and cells enlarge and differentiate into specialized cell types. The molecular mechanism underlying the activation and maintenance of cell proliferation in the apical meristems is unknown. Possible mechanisms for the spatial regulation of cell proliferation and differentiation include a cell-autonomous mechanism propagated from the initial cells to the mitotic progeny (Dolan et al., 1993;Scheres et al., 1994), transport of growth regulators between organs, and the axial polarity generated within the organ. For proliferating cells, passage of a cell .through the cell cycle is regulated by cdc2 protein kinase and cyclin (Hunt, 1991;Scherr, 1993). Genes containing sequence homology to yeast or animal genes encoding proteins such as cdc2 protein kinase, cyclin, and mitogen-activated protein kinase have been isolated from plants (Hemerly et al., 1992;Hirt et al., 1992;Martinez et al., 1992;Mizoguchi et al., 1994). Mutants unable to form shoot meristems, e.g. the shoot mevistemless mutan...

Inactivation of Thioredoxin Reductases Reveals a Complex Interplay between Thioredoxin and Glutathione Pathways in Arabidopsis Development

“…NTRs play a limited role in the root and apical meristem, leading only to a small reduction of growth in the ntra ntrb mutant. By contrast, the low synthesis of glutathione in rml1 completely blocks root meristem growth while the shoot meristem develops (Cheng et al, 1995;Vernoux et al, 2000). Shoot growth in rml1 is almost normal in the first days after germination but is clearly limited later, probably by the low nutrient supply caused by the absence of a root system.…”

“…In order to confirm genetically the role of glutathione in the ntra ntrb mutant, we crossed the ntra ntrb mutant with the rml1 mutant (Cheng et al, 1995). This mutation was shown to segregate as a single recessive allele.…”

Glutathione – linking cell proliferation to oxidative stress

“…The rootmeristemless1 (rml1) mutants were originally identified on the basis of their inability to maintain cell division following germination because the cell cycle arrests in the primary root at an early stage (42,43). The factor required to activate and maintain the cell division in the root apical cells was shown to be GSH (43).…”

Building a root: the control of patterning and morphogenesis during root development.

“…This point has been clearly emphasized by the study of the rootmeristemless (rml7 and rm12) mutations of Arabidopsis (Cheng et al, 1995). Embryogenic root development is normal in these mutants, but cell divisions in the postembryonic root are lacking or greatly reduced, which leads to exceedlingly small roots (Cheng et al, 1995).…”