Plants with modified growth

Details Plants with modified growth Plants with modified growth

1999-09-24

2003-05-06

McElwain, Elizabeth F. (Department: 1638)

Multicellular living organisms and unmodified parts thereof and

Method of introducing a polynucleotide molecule into or...

The polynucleotide alters plant part growth

C800S298000, C435S320100, C435S419000

Reexamination Certificate

active

06559358

ABSTRACT:

This invention relates to the use of cell-division controlling proteins or parts thereof, preferably cell-division controlling proteins that bind retinoblasoma-like proteins, more preferably cyclins, particularly D-type cyclins and genes encoding same, for producing plants with modified phenotypes, particularly plants with modified growth rates or plants comprising parts with modified growth rates and/or modified relative sizes or plants with modified architecture. This invention also relates to plant cells and plants expressing such DNAs.
BACKGROUND TO THE INVENTION
All eukaryotic cells undergo the same sequential series of events when they divide, and the term “cell cycle” reflects the ordered nature and universality of these events. In the eukaryotic cell cycle DNA replication (S) and cell division (M) are normally temporally separated by “gap” phases (G1 and G2) in the sequence G1-S-G2-M. This arrangement allows entry to the critical processes of DNA replication and mitosis to be precisely controlled. Underlying the cytological events of the cell cycle is an ordered series of temporally and spatially organised molecular and cellular processes which define the direction and order of the cycle. Cell cycle progression appears to be regulated in all eukaryotes by major controls operating at the G1-to-S phase and G2-to-M phase boundaries. Passage through these control points requires the activation of cyclin-dependent kinases (CDKs), whose catalytic activity and substrate specificity are determined by specific regulatory subunits known as cyclins and by interactions with other proteins that regulate the phosphorylation state of the complex (reviewed in Atherton-Fessier et al., 1993; Solomon, 1993). In budding and fission yeasts, both the G1-to-S and G2-to-M phase transitions are controlled by a single CDK, encoded by the cdc2+ gene in
Schizosaccharomyces pombe
and by CDC28 in
Saccharomyces cerevisiae
. The association of p34
cdc2
(p34
CDC28
in budding yeast) with different cyclin partners distinguishes the two control points (reviewed in Nasmyth, 1993). In mammalian cells, a more complex situation prevails, with at least six related but distinct CDKs (encoded by cdc2/cdk1, cdk2, cdk3, cdkain 4, cdk5, and cdk6) having distinct roles, each in conjunction with one or more cognate cyclin partners (Fang and Newport, 1991; Meyerson et al., 1991, 1992; Xiong et al., 1992b; Tsai et al., 1993a; van den Heuvel and Harlow, 1993; Meyerson and Harlow, 1994). B-type cyclins are the major class involved in the G2-to-M transition and associate with p34
cdc2
or its direct homologs (reviewed in Nurse, 1990). Cyclin B is one of two cyclins originally described as accumulating in invertebrate eggs during interphase, and rapidly destroyed in mitosis (Evans et al., 1983), and it is a component of Xenopus maturation-promoting factor (Murray et al., 1989). Subsequently, cyclin B homologs have been identified from many eukaryotic species. Cyclin A is also of widespread occurrence in multicellular organisms, and its precise role is unclear, although its peak of abundance suggests a function in S phase (reviewed in Pines, 1993).
The G1-to-S phase transition is best understood in
S. cerevisiae
. Genetic studies define a point late in G1 called START. After passing START, cells are committed to enter S phase and to complete a full additional round of division, which will result in two daughter cells again in G1 phase (Hartwell, 1974; reviewed in Nasmyth, 1993). The products of three
S. cerevisiae
G1 cyclin genes called CLN1, CLN2, and CLN3 are the principal limiting components for passage through START (Richardson et al., 1989; Wittenberg et al., 1990; Tyers et al., 1993). Transcription of CLN1 and CLN2 is activated in G1, and accumulation of their protein products to a critical threshold level by a positive feedback mechanism leads to activation of the p34
CDC28
kinase and transition through START (Dirick and Nasmyth, 1991). The G1 cyclins are then degraded as a consequence of PEST motifs in their primary sequence that appear to result in rapid protein turnover (Rogers et al., 1986; Lew et al., 1991; reviewed in Reed, 1991).
The
S. cerevisiae
G1 cyclins are at least partially redundant, because yeast strains in which two of the three G1 cyclin genes are deleted and the third placed under the control of a galactose-regulated promoter show a galactose-dependent growth phenotype. Such strains have been used to identity Drosophila and human cDNA clones that rescue this conditional cln-deficient phenotype on glucose plates when the single yeast CLN gene present is repressed (Koff et al., 1991; Lahue et al., 1991; Leopold and O'Farrell, 1991; Lew et al., 1991; Xiong et al., 1991). Human cDNAs encoding three new classes of cyclins, C, D, and E, were identified by this means. Although these cyclins show only limited homology with the yeast CLN proteins, they have proved important for understanding controls that operate in mammalian cells during G1 and at the restriction point at the G1-to-S phase boundary (Pardee, 1989; Matsushime et al., 1992; Koff et al., 1992, 1993; Ando et al., 1993; Quelle et al., 1993; Tsai et al., 1993b). Cyclin E may act as a rate-limiting component at the G1-to-S phase boundary (Ohtsubo and Roberts, 1993; Wimmel et al., 1994), whereas the dependency of cyclin D levels on serum growth factors (Matsushime et al., 1991; Baldin et al., 1993; Sewing et al., 1993) suggests that cyclins of the D-type may form a link between these signals and cell cycle progression.
An important factor involved in the regulation of cell cycle progression in mammals is the retinoblastoma susceptibility gene encoding the retinoblastoma protein (Rb). Rb binds and inactivates the E2F family of transcription factors, and it is through this ability that Rb exerts most of its potential to restrain cell division in the G1-phase. E2F transcription factors are known to switch on cyclin E and S-phase genes and the rising levels off cyclin E and/or E2F lead to the onset of replication (Nevins, 1992, Johnson et al., 1993). The ability of Rb to inactivate E2F depends on its phosphorylation state. During most of G1, Rb is in a hypophosphorylated state, but in late G1 phase, phosphorylation of Rb is carried out by cyclin-dependent kinases particularly CDK4 complexed to its essential regulatory subunit, cyclin D (Pines, 1995) and CDK2 complexed to cyclin E (at the G1/S boundary) or cyclin A (in S phase). These multiple phosphorylations of Rb cause it to release E2F, which can then, ultimately promote transcription of the S-phase genes.
Plant cells were used in early studies of cell growth and division to define the discrete phases of the eukaryotic cell cycle (Howard and Pelc, 1953), but there is a paucity of data on molecular cell cycle control in plant systems. Plant cells that cease dividing in vivo due to dormancy, or in vitro due to nutrient starvation, arrest at principal control points in G1 and G2 (van't Hof and Kovacs, 1972; Gould et al., 1981; reviewed in van't Hof, 1985); this is in general agreement with the controls operating in other eukaryotic systems. Although mature plant cells may be found with either a G1 or a G2 DNA content (Evans and van't Hof, 1974; Gould et al., 1981), the G1 population generally predominates. The G1 control point is found to be more stringent in cultured plant cells subjected to nitrogen starvation; these cells arrest exclusively in G1 phase (Gould et al., 1981). Strong analogies thus exist between the principal control point in G1 of the plant cell cycle, the START control in yeasts, and the restriction point of mammalian cells.
Antibodies or histone HI kinase assays have been used to indicate the presence and localization of active CDC2-related kinases in plant cells (John et al., 1989,1990, 1991; Mineyuki et al., 1991; Chiatante et al., 1993; Colasanti et al., 1993; reviewed in John et al., 1993), and cDNAs encoding functional homologs of CDC2 kinase have been isolated by reduced stringency hybridization or redundant polymerase chain reaction from

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