Eight microsatellite loci were characterized within two cultivated beet (Beta vulgaris ssp. vulgaris) accessions and one accession of the wild progenitor of domesticated sugar beet, Beta vulgaris ssp. maritima. Allele diversity was high, yielding two to 11 alleles per locus. Polymorphism information content (PIC) values obtained for these eight loci where also high and indicate the highly informative nature of the microsatellites presented here. These described markers add to a small set of publicly available microsatellite markers for beet and will be instrumental in identifying patterns of genetic diversity and origins of domestication.

The present study demonstrates that postnatal ID produces long-lasting impairments in dopaminergic-dependent synaptic plasticity in the hippocampus. These impairments may play a role in the learning and memory deficits known to result from ID.

Yme1p, an ATP-dependent protease localized in the mitochondrial inner membrane, is required for the growth of yeast lacking an intact mitochondrial genome. Specific dominant mutations in the genes encoding the α- and γ-subunits of the mitochondrial F1F0-ATPase suppress the slow-growth phenotype of yeast that simultaneously lack Yme1p and mitochondrial DNA. F1F0-ATPase activity is reduced in yeast lacking Yme1p and is restored in yme1 strains bearing suppressing mutations in F1-ATPase structural genes. Mitochondria isolated from yme1 yeast generated a membrane potential upon the addition of succinate, but unlike mitochondria isolated either from wild-type yeast or from yeast bearing yme1 and a suppressing mutation, were unable to generate a membrane potential upon the addition of ATP. Nuclear-encoded F0 subunits accumulate in yme1 yeast lacking mitochondrial DNA; however, deletion of genes encoding those subunits did not suppress the requirement of yme1 yeast for intact mitochondrial DNA. In contrast, deletion of INH1, which encodes an inhibitor of the F1F0-ATPase, partially suppressed the growth defect of yme1 yeast lacking mitochondrial DNA. We conclude that Yme1p is in part responsible for assuring sufficient F1F0-ATPase activity to generate a membrane potential in mitochondria lacking mitochondrial DNA and propose that Yme1p accomplishes this by catalyzing the turnover of protein inhibitors of the F1F0-ATPase.

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