Biomedical subjects
J Ogas
Publications and source records attributed to J Ogas.
PICKLE is a CHD3 chromatin-remodeling factor that regulates the transition from embryonic to vegetative development in Arabidopsis.
The life cycle of angiosperms is punctuated by a dormant phase that separates embryonic and postembryonic development of the sporophyte. In the pickle (pkl) mutant of Arabidopsis, embryonic traits are expressed after germination. The penetrance of the pkl phenotype is strongly enhanced by inhibitors of gibberellin biosynthesis. Map-based cloning of the PKL locus revealed that it encodes a CHD3 protein. CHD3 proteins have been implicated as chromatin-remodeling factors involved in repression of transcription. PKL is necessary for repression of LEC1, a gene implicated as a critical activator of embryo development. We propose that PKL is a component of a gibberellin-modulated developmental switch that functions during germination to prevent reexpression of the embryonic developmental state.
Dissecting the gibberellin response pathway.
The recent cloning of three Arabidopsis genes that regulate the response to gibberellin - one of the five 'classical' plant hormones - provides the first glimpse of possible molecular mechanisms operating in gibberellin signal transduction in plants.
Cellular differentiation regulated by gibberellin in the Arabidopsis thaliana pickle mutant.
The plant growth regulator gibberellin (GA) has a profound effect on shoot development and promotes developmental transitions such as flowering. Little is known about any analogous effect GA might have on root development. In a screen for mutants, Arabidopsis plants carrying a mutation designated pickle (pkl) were isolated in which the primary root meristem retained characteristics of embryonic tissue. Expression of this aberrant differentiation state was suppressed by GA. Root tissue from plants carrying the pkl mutation spontaneously regenerated new embryos and plants.
Cell cycle control by a complex of the cyclin HCS26 (PCL1) and the kinase PHO85.
The events of the eukaryotic cell cycle are governed by cyclin-dependent kinases (cdk's), whose activation requires association with cyclin regulatory subunits expressed at specific cell cycle stages. In the budding yeast Saccharomyces cerevisiae, the cell cycle is thought to be controlled by a single cdk, CDC28. Passage through the G1 phase of the cell cycle is regulated by complexes of CDC28 and G1 cyclins (CLN1, CLN2, and CLN3). A putative G1 cyclin, HCS26, has recently been identified. In a/alpha diploid cells lacking CLN1 and CLN2, HCS26 is required for passage through G1. HCS26 does not associate with CDC28, but instead associates with PHO85, a closely related protein kinase. Thus, budding yeast, like higher eukaryotes, use multiple cdk's in the regulation of cell cycle progression.
The PCL2 (ORFD)-PHO85 cyclin-dependent kinase complex: a cell cycle regulator in yeast.
Cyclin-dependent kinase (cdk) complexes are essential activators of cell cycle progression in all eukaryotes. In contrast to mammalian cells, in which multiple cdk's contribute to cell cycle regulation, the yeast cell cycle is largely controlled by the activity of a single cdk, CDC28. Analysis of the putative G1 cyclin PCL2 (ORFD) identified a second cyclin-cdk complex that contributes to cell cycle progression in yeast. PCL2 interacted with the cdk PHO85 in vivo and in vitro and formed a kinase complex that had G1-periodic activity. Under genetic conditions in which the Start transition was compromised, PHO85 and its associated cyclin subunits were essential for cell cycle commitment. Because PHO85 and another cyclin-like molecule, PHO80, also take part in inorganic phosphate metabolism, this cdk enzyme may integrate responses to nutritional conditions with the cell cycle.
Transcriptional activation of CLN1, CLN2, and a putative new G1 cyclin (HCS26) by SWI4, a positive regulator of G1-specific transcription.
SWI4 of budding yeast codes for a component of a transcription factor (cell cycle box factor, or CCBF) necessary for G1-specific expression of HO. We show that SWI4 is essential for haploid cell viability at high temperature and in a/alpha cells at all temperatures: SWI4-deficient cells arrest as large unbudded cells. Eight high copy number plasmids were identified that allow swi4- strains to grow under nonpermissive conditions. Two carry G1 cyclin genes, CLN1 and CLN2; another carries HCS26, coding for a putative cyclin, a/alpha swi4- mutants exhibit 3- to 20-fold reductions in the levels of CLN1, CLN2, and HCS26 transcripts. The requirement of SWI4 for transcription appears to be direct: each gene contains sites similar to the CCBF-binding site; CCBF binds to the upstream region of HCS26. We propose that SWI4 participates in a positive feedback loop by which CLN1, CLN2, and possibly HCS26 promote their own transcription in G1.
Regulators of synthesis and activity of the G1 cyclins of budding yeast.
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