High impact information on APA1

• HMR-E sequences and targeted Sir4, both of which cause late replication of ARS305, also cause transcriptional silencing of the nearby APA1 gene.CONCLUSIONS: Sir proteins are sufficient to reprogram an origin from early to late; that is, Sir proteins are a cause of late replication [1].
• Deletion of APA1 causes a defective regulation of the PMA1 expression by glucose but has not noticeable effect on the expression of other TUF-regulated genes [2].
• We have now used the AC method to map APA1 gene to a site 44 kb from the left terminus of the chromosome, between the HIS4 and HML genes [3].
• This location was confirmed by the comparison of restriction maps of the APA1 gene region to published restriction maps of chromosome III [3].
• Intracellular Ap4A increased 3- to 20-fold during growth on galactose of a transformant with APA1 under the control of the GAL1 promoter [4].

Biological context of APA1

• Enhanced expression of APA1 via the plasmids resulted in 10- and 90-fold increases in Ap4A phosphorylase activity, respectively, as assayed in vitro [4].
• The chromosomal locus of APA1 has been disrupted in a haploid strain [4].
• The paradoxical increase in Ap4A upon enhanced expression of APA1 indicates that the metabolic consequences of altered gene expression may be more complex than indicated solely by assay of enzymatic activity of the gene product [4].

Associations of APA1 with chemical compounds

• These results suggest a model in which APA1 acts on a glucose-signaling pathway that controls the expression of several genes that are transcriptionally regulated by glucose [2].

Other interactions of APA1

• Disruption of APA2 and/or APA1 shows that none of these genes is essential for the viability of Saccharomyces cerevisiae [5].
• APA1 has been inserted into a multicopy plasmid and into a centromeric plasmid with a GAL1 promoter [4].

References