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Biomedical subjects

S R Spindler

Publications and source records attributed to S R Spindler.

At least 19 recordsLinked to original sources

Positive and negative thyroid hormone response elements are composed of strong and weak half-sites 10 nucleotides in length.

The steroid-thyroid hormone receptors bind to imperfect repeats of two or more half-sites. It is generally accepted that a T3 response element (TRE) half-site consists of a six-nucleotide core motif (5'-AGGT(C/A)A-3'). It is less widely appreciated that the nucleotides flanking this core motif also have a major influence on the affinity of T3 receptor (TR) for its response element. We analyzed TR-DNA interactions under conditions in which the affinity of receptor monomers for individual TRE half-sites of the rat GH (rGH) gene was measured. These studies avoided the effects of half-site spacing and orientation on receptor binding. Variations in the nucleotides flanking the core sequence can modulate receptor binding by more than 15-fold. Systematic mutational analysis of TRE half-site structure demonstrated that at least two nucleotides flanking either side of the half-site core motif strongly influence TR binding affinity and activity, indicating that half-sites are approximately 10 nucleotides long. Thus, the half-sites of most TREs overlap, and mutations in one half-site may affect the activity of its partner. The TRE half-site sequence 5'-CTGAGGTAACG-3' was bound with highest affinity by TRs. The negatively T3-responsive promoter of the rGH gene was used to investigate the functional significance of the nucleotides flanking the core motif in vivo. A promoter consisting of only 22 rGH nucleotides, containing two functional TRE half-sites which overlap the rGH TATA box, directed T3-inhibited transcription. Mutation of nucleotides flanking the core sequence of the weaker half-site dramatically reduced the activity of the element, demonstrating that the flanking sequences of the half-sites can profoundly affect TRE activity.

Animals

Aging alters hepatic expression of insulin receptor and c-jun mRNA in the mouse.

The clear association between species and life span suggests that aging, like development, is genetically orchestrated. To explore this hypothesis, the expression of mRNA for a number of transcription regulatory and signal transduction proteins was investigated during aging of B10.RIII, C57BL/10 and B10.BR mice. mRNA for glucocorticoid receptor, CCAAT and enhancer binding protein, transcription factor Sp1 and RNA polymerase II elongation factor S-II were unchanged between 4 and 24 months of age in these mice. These factors are required for the normal transcription of many genes, perhaps explaining their steady rates of expression throughout life. Insulin-like growth factor I mRNA also remained unchanged. By contrast, mRNA for the insulin receptor and transcription factor c-jun changed significantly during aging. c-Jun mRNA decreased approximately 55% between 4 and 12 months of age and then increased by 24-25 months of age to levels approximately equal to those found in young mice. Insulin receptor mRNA increased approximately 30% by 24-25 months of age in all strains of mice. These results suggest that factors determining the steady state level of these mRNAs are altered in level or activity during aging. Assessing the causes and significance of these changes will require further study. However, our results demonstrate that alterations in the expression of specific regulatory genes occur during aging.

Aging

Influence of age and caloric restriction on expression of hepatic genes for xenobiotic and oxygen metabolizing enzymes in the mouse.

The influence of age and life-span-prolonging caloric restriction on the expression of hepatic genes for xenobiotic and activated oxygen metabolism was investigated in female C3B10RF1 mice, a long-lived hybrid strain. Animals were fed either ad libitum, or diets reduced 20% or 52% in total calories but approximately unchanged in total protein, vitamins, and minerals. Cytochrome P1- and P3-450 (cyp1A1 and cyp1A2, respectively) mRNA levels decreased approximately 40% between age 4-5 months (young) and 30-31 months (old) in ad libitum fed animals (p less than or equal to .05). Caloric restriction eliminated this decrease. Manganese-superoxide dismutase mRNA decreased significantly in old ad libitum fed mice, and caloric restriction eliminated this decrease. No change in manganese-superoxide dismutase activity was detected, probably due to its low level and the large variability inherent in the assay. Catalase mRNA increased with age, but was not affected by diet. Catalase activity increased significantly with caloric restriction in young and old mice, in the absence of an increase in catalase mRNA, suggesting translational or posttranslational effects. CuZn-superoxide dismutase, glutathione peroxidase and epoxide hydrolase mRNA, and the ratio of ribosomal to total mRNA did not change with age or diet.

Aging

Aging and restriction of dietary calories increases insulin receptor mRNA, and aging increases glucocorticoid receptor mRNA in the liver of female C3B10RF1 mice.

We investigated the influence of age and a 20% or 52% reduction in dietary calories (caloric restriction) on expression of mRNA for a number of transcription factors and signal-transducing proteins using 4, 16, and 30-month-old female mice of the long-lived C3B10RF1 strain. In all age groups, 52% caloric restriction, which extends maximum life span by approximately 33%, increased insulin receptor mRNA by 15% to 25% over the levels in animals fed ad libitum. Aging increased insulin receptor mRNA and glucocorticoid-receptor mRNA in all dietary groups. A similar increase in glucocorticoid receptor mRNA was not observed for male mice of three other strains, suggesting the change is sex- or strain-specific and not a general feature of aging. These changes appear to be specific. Neither caloric restriction nor age had an effect on the level of mRNA for insulin-like growth factor-I, RNA polymerase II elongation-factor S-II, or transcription factors Sp1, CCAAT and enhancer binding protein, or proto-oncogene c-jun.

Aging

Alpha and beta thyroid hormone receptors bind immediately adjacent to the rat growth hormone gene TATA box in a negatively hormone-responsive promoter region.

We report that alpha and beta type rat thyroid hormone receptors bind specifically and with high affinity to the 10-base pair sequence immediately 3' of the rat growth hormone TATA box (positions -25 to -16) in a region of the rat growth hormone promoter which can be negatively hormone responsive (nTRE). The receptors have approximately 7-fold lower affinity in vitro for the nTRE than for the thyroid hormone-responsive enhancer of the rat growth hormone gene (TRE). Proteins extracted with high salt concentration from rat pituitary cell nuclei enhance binding of the receptors to both the TRE and nTRE. A modification of the avidin-biotin complex DNA binding assay which enhances the sensitivity of the assay approximately 100-fold was used in these studies. The immediate proximity of a receptor binding site to the rat growth hormone TATA box suggests that direct interaction between receptor and TFIID (the TATA binding protein) mediates nTRE activity.

Animals

Age-related down regulation of hepatic cytochrome P1-450, P3-450, catalase and CuZn-superoxide dismutase RNA.

The influence of age on liver gene expression was investigated in two strains of H-2 congenic mice. In B10.RIII mice (H-2r), basal P1- and P3-450 RNA levels progressively decreased 65 and 95%, respectively, between 4 and 28 months of age (P less than or equal to 0.05). Polyaromatic hydrocarbon (PAH) induced P1- and P3-450 RNA levels decreased about 50% during this time (P less than or equal to 0.05). In contrast, in C57BL/10 mice (H-2b) little or no change was detected in basal or induced P1- or P3-450 RNA levels. CuZn-superoxide dismutase RNA decreased 80 to 90% between 4 and 9 months of age in B10.RIII mice, while a quantitatively smaller decrease of 50 to 65% was found in C57BL/10 mice (P less than or equal to 0.05). Catalase RNA decreased approximately 80% between 4 and 9 months of age in B10.RIII mice, and a similar decrease was found in C57BL/10 mice. Down regulation of these genes may explain the reduced activities of the cognate hepatic enzymes, and reduced xenobiotic metabolism found in older animals.

Aging

Dietary energy restriction in mice reduces hepatic expression of glucose-regulated protein 78 (BiP) and 94 mRNA.

The influence of life span-prolonging dietary energy restriction on hepatic expression of glucose-regulated protein 78 and 94 (GRP78 and GRP94) RNA was investigated in female C3B10RF1 mice. Mice were either fed ad libitum or fed diets reduced 20 or 40% in energy but containing approximately equivalent amounts of protein, fats, vitamins and minerals. Aging produced no changes in GRP mRNA. However, GRP78 and GRP94 mRNA levels were reduced approximately 50 and 40%, respectively, by 40% energy restriction. This level of energy restriction produced a 43% reduction in the mean plasma glucose levels of young and old mice. The changes in GRP mRNA expression appear to be specific, because the levels of these RNAs were normalized to the level of polyadenylated RNA, and no changes were detected in the levels of a number of other mRNAs. Although extreme glucose deprivation increases GRP mRNA levels in cultured cell lines, physiologically relevant reductions in blood glucose had the opposite effect in the liver, in vivo. The regulatory pathway responsible for these effects is not known. GRP mRNA levels are elevated by agents that increase the level of malfolded proteins in the endoplasmic reticulum. Thus, energy restriction may act to reduce malfolded proteins in the endoplasmic reticulum of hepatic cells.

Aging

P1-450 and P3-450 gene expression and maximum life span in mice.

The effects of beta-naphthoflavone on the inducibility of hepatic P1-450 and P3-450 mRNA were investigated in male B10.RIII/Sn, C57BL/10Sn, C3H/HeSnJ, and A/WYSn mice. Previous work has shown that the maximum level of aryl hydrocarbon hydroxylase induction in these strains correlates with maximum life span. In this study we found that the maximum inducible levels of P1- and P3-450 RNA were significantly different among the strains, and these levels also correlate with life span. The differences were not due to strain-specific differences in the kinetics of P1- or P3-450 RNA induction. The differences were specific to expression of the P-450 genes, since the levels of hepatic alpha-actin and albumin RNA were not significantly different among the strains, and specific RNA levels were normalized to the level of total polyadenylated RNA. beta-Naphthoflavone was found to induce alpha-actin mRNA approximately 2-fold and to transiently repress albumin RNA about 50% in all mouse strains. Maximum P1- and P3-450 gene expression correlated directly with the 10th deciles of survival of the mouse strains. Longer-lived strains expressed higher combined levels of P1- and P3-450 RNAs. Maximum P1- and P3-450 gene expression also correlated generally with the reported aryl hydrocarbon hydroxylase receptor levels of each strain. It is unlikely that the hepatic P1- and P3-450 genes are ever maximally induced under the sheltered laboratory conditions used to determine maximum life span, as we consistently find very low levels of P-450 expression in uninduced animals. These uninduced levels were not statistically different between the strains. Therefore, the reason for the relationship between maximum life span and maximum P1- and P3-450 inducibility is unclear at present.

Actins

Thyroid hormone transcriptional regulatory region of the growth hormone gene.

By deletion-transfection analysis, a region of the rat growth hormone gene has been identified which directs accurate, thyroid hormone responsive transcriptional initiation in vivo. In addition, a thyroid hormone-responsive DNase I hypersensitive domain containing three discrete hypersensitive sites has been identified near the GH promoter. One site is coincident with the TATA homology, and the others lie approximately 150 nucleotides 5' and 3' of this sequence. The TATA and 5' flanking DNA hypersensitive sites are located in the region of the gene which promotes hormone-responsive gene transcription. Based on these results, it is possible that the molecular basis for thyroid hormone induction of GH gene transcription includes binding of the occupied receptor to chromatin sites flanking the TATA homology, promoting binding of the TATA activating protein to this sequence. Together, these events may enhance the rate of RNA polymerase II initiation at the promoter.

Animals

Sequences essential for activity of the thyroid hormone responsive transcription stimulatory element of the rat growth hormone gene.

Thyroid hormone dependent transcription stimulatory and inhibitory elements exist at the 5'-end of the rat GH (rGH) gene (TSE and TIE, respectively). In this study, the location of the sequences essential for TSE activity was examined using stably transfected GC cells. Because the TIE may influence TSE activity, we investigated TSE activity both on the rGH promoter, in the presence of the TIE, and on the viral thymidine kinase promoter, with the TIE deleted. The results of these studies indicate that the minimum sequences essential for TSE activity exist between positions -194 and -169 of the rGH gene.

Animals

Discrete positive and negative thyroid hormone-responsive transcription regulatory elements of the rat growth hormone gene.

We have recently shown that a thyroid hormone-responsive transcription stimulatory element exists in the 5'-flanking DNA near the rat growth hormone (rGH) gene (Crew, M. D., and Spindler, S. R. (1986) J. Biol. Chem. 261, 5018-5022). Progressive deletion-transfection analysis of the 5' end of the gene has led to the identification of two genetic elements responsive to thyroid hormone. The first of these is a thyroid hormone-responsive transcription stimulatory element, or TSE. The TSE induced a thyroid hormone-dependent induction-attenuation transcription cycle similar to that of the natural rGH gene. Deletion of sequences between positions -254 and -241 in the rGH 5'-flanking DNA eliminated TSE activity. The second regulatory element is a thyroid hormone-responsive transcription inhibitory element (TIE). When this element was active, thyroid hormone strongly but transiently inhibited rGH promoter utilization. Deletion of sequences between nucleotides -46 and -21 abolished the effects of the TIE. To determine whether the TSE and TIE are enhancer-like, we ligated various regions of rat growth hormone 5'-flanking DNA containing these elements to a chimeric test gene containing the Herpes simplex virus thymidine kinase promoter. Thyroid hormone activated heterologous promoter utilization when a rat growth hormone 5'-flanking DNA fragment containing the TSE (-520 to -115) was linked in cis, regardless of the distance or orientation of the TSE with respect to the promoter. These data suggest that the TSE is a thyroid hormone-dependent enhancer. In contrast, when the TIE was placed immediately 5' to the thymidine kinase promoter, transcription was not effected by 3,5,3'-L-triiodothyronine, suggesting that the TIE is not enhancer-like.

Animals

Age-related decrease of growth hormone and prolactin gene expression in the mouse pituitary.

The effects of aging on pituitary GH, PRL, and alpha-tubulin messenger RNA (mRNA) levels were measured in 3-, 12-, and 27-month-old male C57BL/6J mice by dot-blot hybridization. The amount of GH and PRL mRNA in the pituitary deceased dramatically with age. However, total poly(A+) RNA (mRNA), as measured by hybridization with radioactively labeled oligo-(dT), was not altered during aging. In addition, there were no age-related changes in the level of alpha-tubulin mRNA. Thus, the effects of aging on GH and PRL mRNA levels are specific; the levels of the majority of cellular mRNAs are not altered with age. GH and mRNA levels decreased 35% between 3 and 12 months (P less than 0.05) and a total of 75% after 27 months (P less than 0.01). PRL mRNA levels decreased 65% between 12 and 27 months (P less than 0.01), although there was no significant decrease before 12 months. Whereas T3 is the most potent regulator of GH gene expression, we did not detect any significant age-related change in serum T3 levels. These results suggest that factors other than T3 play a role in the age-related decline in GH and PRL gene expression.

Aging

Alterations in local chromatin structure accompany thyroid hormone induction of growth hormone gene transcription.

The chromatin structure of the growth hormone gene and flanking DNA was analyzed in GC rat pituitary tumor cells, which appropriately express and regulate the gene. Thyroid hormone induced the DNase I hypersensitivity of a chromatin domain spanning the transcriptional initiation site from approximately -200 to +150. Three inducible hypersensitive sites were discerned in this region. One of these sites was in the first intron of the gene. The second site was within a region of 5' flanking DNA which promotes accurate, thyroid hormone-regulated transcriptional initiation. Centered between these two sites was a third hormone-inducible hypersensitive site mapping at the position of the TATA sequence. The hormone responsiveness of these hypersensitive sites suggests that occupied 3,5,3'-triiodo-L-thyronine receptor interacts with sequences flanking the growth hormone promoter, perhaps facilitating the binding or activation of a transcription factor at the TATA homology. Three hormone-independent hypersensitive sites were identified near or within intron or flanking DNA sequences similar to Chinese hamster ovary type 2 repetitive DNA. Two additional hormone-independent hypersensitive sites were located more than 1000 nucleotides up-stream of the growth hormone promoter. These sites were present in the cloned genomic DNA and were the only distinct sites found in rat spleen and cultured rat liver cells. Thyroid hormone treatment of GC cells appeared to increase the moderate DNase I sensitivity of the growth hormone gene region beyond that found in deinduced or glucocorticoid-treated cells. Dexamethasone had no discernible effect on the chromatin structure of the gene or flanking DNA in these studies.

Animals

Thyroid hormone regulation of the transfected rat growth hormone promoter.

A region of the rat growth hormone gene and 5' flanking DNA has been identified which promotes accurate, thyroid hormone-regulated transcriptional initiation. GC rat pituitary tumor cells were transfected with chimaeric plasmids containing various lengths of rat growth hormone gene and 5' flanking DNA fused to the coding region of the dominant selectable marker gene neo. Thyroid hormone induction of rGH-neo RNA was observed by Northern and dot blot analysis of cells transfected with rGH-neo chimaeric genes sharing the rat growth hormone gene and upstream regions from -235 to +11. Initiation of rGH-neo transcription was mapped by S1 nuclease protection to the in vivo initiation site of the natural growth hormone gene. Transcription of the most deleted thyroid hormone responsive construct involved an induction-attenuation cycle qualitatively similar to the response of the natural gene. However, the 3,5,3'-triiodo-L-thyronine responsiveness of this deleted construct was approximately 2- to 3-fold less than that of less deleted rGH-neo genes tested. These results suggest that, at a minimum, the sequences required for the cyclic 3,5,3'-triiodo-L-thyronine transcriptional response are located within the region of the gene from -235 to +11. Other sequences essential for full responsiveness appear to be located elsewhere in the 5'-flanking DNA. Rat growth hormone promoter utilization appears to be strongly cell-type dependent. We obtained stable transfectants with rGH-neo constructs only in GC cells.

Animals

A computer method for scanning and analysis of dot blots.

A system is described for computer analysis of autoradiograms produced from dot blots. The autoradiograms are first digitized on a rotating drum densitometer. The system automatically locates, integrates, and corrects the intensity of each spot for background. A linear range of exposures for each series of dilutions on the dot blot is calculated, and the amount of specific RNA is reported relative to other samples or to an internal standard. Without operator intervention, the system can directly scan and analyze all possible spots produced by the commercial filtration devices which use the geometry of a 96-well microtiter plate.

Computers

Cyclic regulation of growth hormone gene transcription in vivo and in vitro.

The in vivo thyroid and glucocorticoid hormone regulation of GH gene transcription was compared with that found in cultured GH rat pituitary tumor cells. The GH cell lines have been widely used to study GH gene expression, but their relevance to the in vivo regulation of the gene has not been well established. The in vivo studies described here utilized rats that were both thyroparathyroidectomized and adrenalectomized to remove the organ sources of these hormones. The in vitro studies described utilized GC cells hormonally deinduced in medium lacking the hormones. Continuous administration of glucocorticoid or thyroid hormones to either system induced multiple cycles of GH transcriptional activation and deactivation. These cycles were accompanied by cycles of increasing and decreasing GH messenger RNA. In both systems, a brief transcription cycle occurred within hours of thyroid or glucocorticoid hormone addition, and a second broad occurred between 3 and 11 days later. These cycles were independent of changes in receptor levels. The similarities in the responses found in vivo and in cell culture suggest that the molecular mechanisms regulating expression of the GH gene appropriately function in GC cells, despite their transformed phenotype and prolonged maintenance in culture. Thus, these cell lines appear to be appropriate model systems for studies of thyroid and glucocorticoid hormone action.

Animals