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Daniel Pomp

Publications and source records attributed to Daniel Pomp.

23 records · Page 2Linked to original sources

Differential expression of NAT1 translational repressor during development of bovine intramuscular adipocytes.

This study was undertaken to test for differential gene expression in intramuscular adipocytes during fat deposition of feedlot steers. Angus x Hereford steers (n = 50) were fed a high-energy concentrate ration ad libitum for 20 (n = 5), 86 (n = 15), 121 (n = 15), and 146 days (n = 15) to obtain various degrees of intramuscular adipocyte development. Carcass traits were significantly different (P < 0.05) between the groups. Intramuscular adipose tissue was excised from the longissimus dorsi and snap frozen in liquid nitrogen. Pooled samples of total RNA representing each group were analyzed by differential-display polymerase chain reaction using 200 primer combinations comprising 20 arbitrary (5') and 10 anchor (3') oligonucleotides. Bands (n = 70) representing putative differences among treatment groups were excised, sequenced, and subjected to BLAST homology search. From these, 40 contained significant homology to known genes. One was of particular interest, the translational repressor NAT1 (novel APOBEC-1 target-1). NAT1 mRNA was quantified in individual animals to confirm differential expression among treatment groups. Results indicate that NAT1 message is more abundant (P < 0.05) in intramuscular adipocytes of younger/leaner animals.

Adipocytes↗

Pleiotropy of quantitative trait loci for organ weights and limb bone lengths in mice.

We investigated the genetic basis of several limb bone lengths and weights of organs in mice produced from a cross of the F1 between CAST/Ei (wild strain) and M16i (selected for rapid growth rate) back to M16i. From previous correlation studies, we hypothesized that quantitative trait loci (QTLs) would exhibit greater pleiotropy within than between the limb length and organ weight character sets. Using interval mapping procedures and significance testing at the chromosome-wise level, we discovered 14 putative QTLs affecting weight of the liver, spleen, heart, and/or kidney, 9 of which affected more than one organ; and 12 QTLs for limb lengths, all of which affected the length of two or more of the limb bones in these mice. As was hypothesized, most QTLs affected either organ weights or limb lengths independently of each other, although five QTLs were found that affected both sets of characters. The direction of the effect of these QTLs was almost always consistent within and between characters, with little evidence for antagonistic pleiotropy.

Animals↗

The contribution of epistatic pleiotropy to the genetic architecture of covariation among polygenic traits in mice.

The contribution that pleiotropic effects of individual loci make to covariation among traits is well understood theoretically and is becoming well documented empirically. However, little is known about the role of epistasis in determining patterns of covariation among traits. To address this problem we combine a quantitative trait locus (QTL) analysis with a two-locus model to assess the contribution of epistasis to the genetic architecture of variation and covariation of organ weights and limb bone lengths in a backcross population of mice created from the M16i and CAST/Ei strains. Significant epistasis was exhibited by 14 pairwise combinations of QTL for organ weights and 10 combinations of QTL for limb bone lengths, which contributed, on average, about 5% of the variation in organ weights and 8% in limb bone lengths beyond that of single-locus QTL effects. Epistatic pleiotropy was much more common in the limb bones (seven of 10 epistatic combinations affecting limb bone lengths were pleiotropic) than the organs (three of the 14 epistatic combinations affecting organ weights were pleiotropic). In both cases, epistatic pleiotropy was less common than single-locus pleiotropy. Epistatic pleiotropy accounted for an average of 6% of covariation among organ weights and 21% of covariation among limb bone lengths, which represented an average of one-fifth (for organ weights) and one-third (for limb bone lengths) of the total genetic covariance between traits. Thus, although epistatic pleiotropy made a smaller contribution than single-locus pleiotropy, it clearly made a significant contribution to the genetic architecture of variation/covariation.

Animals↗

Genetic variance and covariance patterns for body weight and energy balance characters in an advanced intercross population of mice.

We estimated heritabilities and genetic correlations for a suite of 15 characters in five functional groups in an advanced intercross population of over 2000 mice derived from a cross of inbred lines selected for high and low heat loss. Heritabilities averaged 0.56 for three body weights, 0.23 for two energy balance characters, 0.48 for three bone characters, 0.35 for four measures of adiposity, and 0.27 for three organ weights, all of which were generally consistent in magnitude with estimates derived in previous studies. Genetic correlations varied from -0.65 to +0.98, and were higher within these functional groups than between groups. These correlations generally conformed to a priori expectations, being positive in sign for energy expenditure and consumption (+0.24) and negative in sign for energy expenditure and adiposity (-0.17). The genetic correlations of adiposity with body weight at 3, 6, and 12 weeks of age (-0.29, -0.22, -0.26) all were negative in sign but not statistically significant. The independence of body weight and adiposity suggests that this advanced intercross population is ideal for a comprehensive discovery of genes controlling regulation of mammalian adiposity that are distinct from those for body weight.

Age Factors↗