Fifty-two Angus x Gelbvieh rotationally crossed virgin, ovariectomized, or single-calf heifers were slaughtered after 100 d on a high-concentrate diet. Heifers from each treatment were approximately 31, 33, or 35 mo of age, and they produced 31 A, 5 B, and 16 C maturity carcasses. Because of the small number, B maturity carcasses were not included in this study. Number of A maturity carcasses decreased as age increased. No differences (P > .05) in slaughter weight, total weight gain, dressing percentage, longissimus muscle area, or kidney fat percentage existed between carcass maturity groups, but C maturity heifers had 3.56 mm more fat (P < .01) over the longissimus muscle than A maturity heifers. Marbling scores of slight79 and small0 for A and C maturity carcasses, respectively, did not differ (P > .05). The A and C maturity heifers had similar amounts of collagen and hydroxylysyl-pyridinium crosslinks in metacarpal bone cortex and in longissimus muscle. Neither means for panel tenderness nor Warner-Bratzler shear values differed (P > .05) between maturity groups. Coefficients of variation for tenderness were slightly higher in steaks from C maturity carcasses, but CV for shear values between A and C maturity groups were similar. Because inconsistent meat tenderness is a recognized problem in the beef industry, more research on tenderness variability within maturity and marbling groups is needed. This information, in addition to pooled SEM and differences between means, should aid in finding ways to reduce beef tenderness variability.

Aging↗

PubMed1996

Identification of a novel cis-acting element participating in maximal induction of the human low density lipoprotein receptor gene transcription in response to low cellular cholesterol levels.

In this paper, we present both in vivo and in vitro evidence for the presence of a novel cis-acting regulatory element that is required for maximal induction of the human low density lipoprotein (LDL) receptor gene following depletion of cellular sterols in HepG2 cells. First, in vivo dimethyl sulfate footprinting of the human LDL receptor promoter before and after transcriptional induction in HepG2 cells revealed protection from -145 to -126, 5'-GAGCTTCACGGGTTAAAAAG-3' (referred to as FP1 site). Second, transient transfections of HepG2 cells with promoter luciferase reporter constructs containing the FP1 site resulted in significant enhancement (approximately 375%) of reporter gene expression in response to low levels of sterols compared with parallel plasmid without the FP1 site. In addition, this response was markedly attenuated on nucleotide substitutions within the FP1 site. Third, by electrophoretic mobility shift assays, the FP1 sequence was found to bind protein(s) from HepG2 nuclear extracts in a sequence-specific manner. In vitro binding of the FP1 mutants paralleled the results obtained for their in vivo transcription. On the basis of competition profiles, the FP1-binding factor is different from the known transcription factors binding to the AT-rich CArG and GArC motifs. Furthermore, the FP1-binding protein is not specific to HepG2 cells because nuclear factor(s) with the same specificity was observed in nuclear extracts of non-hepatic HeLa cells. We conclude that transcriptional induction of the LDL receptor gene in response to sterol depletion is mediated, in part, by an highly conserved novel cis-acting element through the binding of specific nuclear protein(s).

Base Sequence↗

PubMed1996