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. 2009 Apr 10;284(15):9625-35.
doi: 10.1074/jbc.X800014200. Epub 2008 Dec 12.

Switching from prokaryotic molecular biology to eukaryotic molecular biology

Masayasu Nomura  1
Affiliations

Switching from prokaryotic molecular biology to eukaryotic molecular biology

Masayasu Nomura. J Biol Chem. .
No abstract available

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Figures

FIGURE 1.
FIGURE 1.
The mentors during my postdoctoral time. a, Sol Spiegelman with his wife, Helen Spiegelman (1958). b, J. D. Watson, S. Benzer, and myself (from left to right) at a meeting in 1990.
FIGURE 2.
FIGURE 2.
Isolation of rrn mutants, which are defective in rRNA synthesis by Pol I. The yeast strain carried ade2 and ade3 mutations and the 2μ-based multicopy plasmid pNOY103. This plasmid carries ADE3 (and URA3 for plasmid selection and counterselection) and the hybrid gene in which the 35 S precursor rRNA coding region is fused to the GAL7 promoter (GAL7-P) and terminator (GAL7-T). It is known that yeast strains carrying ade2 accumulate an intermediate that is converted to a red pigment and that mutation ade3 blocks the pathway to this intermediate, thus preventing the formation of the red pigment. The starting (wild-type (WT)) strain does not form red colonies on rich galactose medium because the plasmid is unstable and not retained in most cells in colonies. Mutants (rrn mutants) that are specifically defective in the Pol I transcription machinery form red colonies on the same rich galactose medium because they can grow only by transcribing the fusion gene by Pol II and hence maintaining the plasmid (which carries ADE3) and accumulating red pigments. The rrn mutants are unable to grow on glucose because transcription from the GAL7 promoter is repressed by glucose.
FIGURE 3.
FIGURE 3.
Model for Pol I transcription initiation from the 35 S rRNA gene promoter. Pol I contains 14 protein subunits. Seven of them are unique to Pol I. Among the genes for these seven, deletion of the genes for two (A34.5 and A14) does not cause any significant growth defects. Mutants carrying alterations in these two genes were not found among rrn mutants, as expected, in the mutant screen shown in Fig. 2. The genes for the remaining five subunits, A190, A135, A12, A43, and A49, were identified as RRN1 (RPA190), RRN2 (RPA135), RRN4 (RPA12), RRN12 (RPA43), and RRN13 (RPA49), respectively, by the rrn mutant screening and were demonstrated to be essential or nearly essential for cell growth. Regarding Pol I transcription factors in mammalian Pol I systems, Rrn3p homologs of human (hRrn3) and mouse (TIFIA) have sequence homology to yeast Rrn3p. Human factor SL1 (and mouse TIFIB) consists of TATA-binding protein (TBP) and three protein subunits. SL1 is functionally homologous to the complex of TATA-binding protein and CF in yeast. However, there is no significant sequence similarity between the three subunits of SL1 and the three subunits of CF. No factor homologous to yeast UAF has been found in mammalian systems thus far.
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