Biomedical subjects

D S Robertson

Publications and source records attributed to D S Robertson.

At least 19 recordsLinked to original sources

PubMed1995

Energy metabolism in weight-stable postobese individuals.

A low metabolic rate for a given body size and body composition and a low ratio of fat to carbohydrate oxidation predict body weight gain. Such metabolic traits could also explain, in part, the propensity of previously obese (postobese) individuals to regain weight after dieting. We studied 11 postobese volunteers (4 males, 7 females; aged 43 +/- 13 y, weighing 80.6 +/- 10.2 kg, with 30 +/- 7% body fat; x +/- SD) who lost 57 +/- 38 kg (23-139 kg) over 14 +/- 12 mo (6-48 mo) on various diet programs and had maintained this weight loss for > or = 2 mo (2-72 mo; 21 +/- 27 mo). After > or = 2 d of a weight-maintenance diet on a metabolic ward, 24-h energy expenditure and ratio of fat to carbohydrate oxidation were measured in a respiratory chamber. Compared with a control group (n = 110) with similar physical characteristics (aged 43 +/- 14 y, weighing 79.5 +/- 11.4 kg, with 30 +/- 12% body fat), [sequence: see text] postobese individuals had similar energy expenditures adjusted for fat-free mass, fat mass, age, and sex, but significantly higher respiratory quotients over 24 h (0.883 +/- 0.026 compared with 0.863 +/- 0.024, P < 0.01) and during sleep, 10 h after the last meal (0.894 +/- 0.063 compared with 0.845 +/- 0.055). These results suggest that postobese individuals have low rates of fat oxidation that may explain their propensity to regain weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed1995

Characterization of the maize gene sugary1, a determinant of starch composition in kernels.

In maize kernels, mutations in the gene sugary1 (su1) result in (1) increased sucrose concentration; (2) decreased concentration of amylopectin, the branched component of starch; and (3) accumulation of the highly branched glucopolysaccharide phytoglycogen. To investigate further the mechanisms of storage carbohydrate synthesis in maize, part of the su1 gene locus and a cDNA copy of the su1 transcript were characterized. Five new su1 mutations were isolated in a Mutator background, and the mutant allele su1-R4582::Mu1 was isolated by transposon tagging. The identity of the cloned element as the su1 gene locus was confirmed by the cosegregation of restriction fragment length polymorphisms in the same or nearby genomic intervals with three additional, independent su1 mutations. Pedigree analysis was also used to confirm the identity of su1. A 2.8-kb mRNA that is homologous to the cloned gene was detected in maize kernels, and a 2.7-kb cDNA clone was isolated based on hybridization to the genomic DNA. Specific portions of the cDNA hybridized with multiple segments of the maize genome, suggesting that su1 is part of a multigene family. The cDNA sequence specified a polypeptide of at least 742 amino acids, which is highly similar in amino acid sequence to bacterial enzymes that hydrolyze alpha-(1-->6) glucosyl linkages of starch. Therefore, debranching of glucopolysaccharides is seemingly part of the normal process of starch biosynthesis, and the final degree of branch linkages in starch most likely arises from the combined actions of branching and debranching enzymes.

Amino Acid Sequence↗

PubMed1994

Genetic analysis of 63 mutations affecting maize kernel development isolated from Mutator stocks.

Sixty-three mutations affecting development of the maize kernel were isolated from active Robertson's Mutator (Mu) stocks. At least 14 previously undescribed maize gene loci were defined by mutations in this collection. Genetic mapping located 53 of these defective kernel (dek) mutations to particular chromosome arms, and more precise map determinations were made for 21 of the mutations. Genetic analyses identified 20 instances of allelism between one of the novel mutations and a previously described dek mutation, or between new dek mutations identified in this study; phenotypic variability was observed in three of the allelic series. Viability testing of homozygous mutant kernels identified numerous dek mutations with various pleiotropic effects on seedling and plant development. The mutations described here presumably arose by insertion of a Mu transposon within a dek gene; thus, many of the affected loci are expected to be accessible to molecular cloning via transposon-tagging.

Alleles↗

PubMed1994

Genetic evidence of Mutator-induced deletions in the short arm of chromosome 9 of maize. II. wd deletions.

Analyses of 113 putative Mutator-induced events involving the yg2 locus of chromosome 9 revealed that 11 of these events were deletions that produce albino seedlings when homozygous. This phenotype is characteristic of wd (white deficiency) deletions. All 11 wd-Mu deletions failed to complement wd1 and pyd1 (pale-yellow deficiency). Nine of the wd-Mu deletions were analyzed cytologically. Two were found to be terminal deletions and seven were internal deletions. Two of the seven had normal pairing throughout the terminal region involved in the pyd1 and wd1 deletions. Because genetic tests established that deletions were present in these two stocks, these deletions were probably too short to disrupt the pairing of the homologous chromosomes. Mechanisms by which the Mutator system might generate these deletions are discussed.

Chromosome Deletion↗

PubMed1993

DNA sequence and transcript analysis of transposon MuA2, a regulator of Mutator transposable element activity in maize.

The 4942 bp DNA sequence of Zea mays transposon MuA2 was determined. Previous evidence indicated MuA2 controls activity of the Mu1 transposon located in the mutable allele a1-mum2. MuA2 contains two large, ATG-initiated open reading frames (ORFs) of 612 and 232 codons, respectively, located on opposite strands. MuA2 produces two transcripts, each containing one of these ORFs. Four different tandem direct repeat sequences are located downstream of the 612 codon ORF. The restriction map of MuA2 is identical to that of transposon MuR1, which also is known to regulate mutability of a1-mum2. Furthermore, except for a single nucleotide, MuA2 is identical to the Mutator element Mu9.

Amino Acid Sequence↗

PubMed1993

Cloning of carotenoid biosynthetic genes from maize.

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Alleles↗

PubMed1991

Feedback theory and Darwinian evolution.

Feedback loops can have a significant impact on biological systems that are evolving under Darwinian natural selection. Many of the striking and sometimes bizarre patterns that characterize the evolution of such systems have simple, natural explanations that involve the effects of feedback loops. The two fundamental types of feedback loops, positive and negative, have effects that are radically different: negative feedback tends to produce stability and resistance to change; positive feedback produces instability and even catastrophe. Both types of feedback loops are important in biological systems, and both can produce chaos, whose mathematical complexity often produces strange, beautiful and totally unexpected patterns that have only begun to be explored using the computational capabilities of modern electronic computers. An understanding of the patterns that can result from the effects of feedback loops can produce important new insights into the patterns that mark the evolutionary development of biological systems.

Animals↗

PubMed1991

Cloning of the Mutator transposable element MuA2, a putative regulator of somatic mutability of the a1-Mum2 allele in maize.

The identification of the autonomous or transposase-encoding element of the Mutator (Mu) transposable element system of maize is necessary to the characterization of the system. We reported previously that a transcript homologous to the internal region of the MuA element is associated with activity of the Mutator system. We describe here the cloning of another Mu element, designated MuA2, that cosegregates with Mutator activity as assayed by somatic instability of the a1-Mum2 allele. The MuA2 element has features typical of the transposable elements of the Mutator family, including the 210-bp terminal inverted repeats. Several lines of evidence suggest that MuA2 is an autonomous or transposase-encoding element of the Mu family: (1) MuA2 cosegregates with a genetically defined element that regulates somatic mutability of the a1-Mum2 allele; (2) MuA2 is hypomethylated while most other MuA2-hybridizing sequences in the genome are extensively methylated; (3) the increase of the copy number of MuA2 is concomitant with the increase of regulator elements; (4) MuA2-like elements are found in Mutator lines but not in non-Mutator inbreds. We propose that autonomous or transposase-encoding elements of the Mu family may be structurally conserved and MuA2-like.

Alleles↗

PubMed1989

Chromosome breakage undetectable in active Mu lines of maize.

We have used a set of Mutator-induced mutants of Bz1 to test whether members of the Mutator (Mu) family of maize transposable elements produce broken chromosomes. From our inability to demonstrate the simultaneous loss of two dominant endosperm markers distal to Mu insertions at Bz1 we conclude that either Mu, unlike many elements of the Ds family, does not induce such breaks, or it does so at a very low frequency.

Alleles↗

PubMed1981