Search PubMed⌕ Search

Biomedical subjects

T D Williams

Publications and source records attributed to T D Williams.

At least 37 records · Page 2Linked to original sources

Interindividual variation in yolk mass and the rate of growth of ovarian follicles in the zebra finch (Taeniopygia guttata).

The amount of resources invested in an individual egg yolk must be determined by its rate of growth and/or the duration of growth. We examined interindividual variation in the growth rate of yolks by injecting radiolabeled amino acid into breeding female zebra finches and measuring the activity associated with protein in the yolks of eggs laid subsequently. We predicted that (1) there would be a positive correlation between yolk mass and the rate of uptake of activity into the yolk; and (2) there would be a negative correlation between clutch size and the amount of activity taken up by each of the follicles due to competition between follicles for circulating yolk precursors. The rate of uptake of activity by the yolks was positively related to yolk mass (r2=0.24, 0.35 and 0.50 for the yolks of the third-, fourth- and fifth-laid eggs, respectively), suggesting that interindividual variation in yolk mass is due, at least in part, to variation in the rate of follicle growth. However, we found no evidence of a trade-off between yolk size and number. The uptake of activity was generally repeatable between breeding attempts (repeatability= 0.23-0.44), as was mean yolk mass (repeatability = 0.35), suggesting that these traits are characteristics of individual females.

Animals↗

Granular corneal dystrophy: slitlamp biomicroscopic appearances in three generations of patients.

PURPOSE: The purpose of this case series is to show photographically the varying clinical appearance of granular corneal dystrophy in three generations of one family and to review the genetic basis of this and related conditions. CASE SERIES: We present cases for four affected individuals along with slitlamp biomicroscopic photographs. DISCUSSION: A review of the photographs and the literature suggests that the abnormal keratoepithelin first appears in the superficial cornea as faint subepithelial opacities. With time, these become arranged in the curved lines of a vortex pattern, after which the deposits become scattered in no particular pattern and at all levels of the cornea. In this family, corneal erosions are a regular feature. Mutations of the gene coding for keratoepithelin (beta ig-h3) may give rise to variable clinical manifestations.

Adolescent↗

Cardiovascular and metabolic responses to fasting and thermoneutrality are conserved in obese Zucker rats.

The primary purpose of the study was to test the hypothesis that reduced leptin signaling is necessary to elicit the cardiovascular and metabolic responses to fasting. Lean (Fa/?; normal leptin receptor; n = 7) and obese (fa/fa; mutated leptin receptor; n = 8) Zucker rats were instrumented with telemetry transmitters and housed in metabolic chambers at 23 degrees C (12:12-h light-dark cycle) for continuous (24 h) measurement of metabolic and cardiovascular variables. Before fasting, mean arterial pressure (MAP) was higher (MAP: obese = 103 +/- 3; lean = 94 +/- 1 mmHg), whereas oxygen consumption (VO(2): obese = 16.5 +/- 0.3; lean = 18.6 +/- 0.2 ml. min(-1). kg(-0.75)) was lower in obese Zucker rats compared with their lean controls. Two days of fasting had no effect on MAP in either lean or obese Zucker rats, whereas VO(2) (obese = -3.1 +/- 0.3; lean = -2.9 +/- 0.1 ml. min(-1). kg(-0.75)) and heart rate (HR: obese = -56 +/- 4; lean = -42 +/- 4 beats/min) were decreased markedly in both groups. Fasting increased HR variability both in lean (+1.8 +/- 0.4 ms) and obese (+2.6 +/- 0.3 ms) Zucker rats. After a 6-day period of ad libitum refeeding, when all parameters had returned to near baseline levels, the cardiovascular and metabolic responses to 2 days of thermoneutrality (ambient temperature 29 degrees C) were determined. Thermoneutrality reduced VO(2) (obese = -2.4 +/- 0.2; lean = -3.3 +/- 0.2 ml. min(-1). kg(-0.75)), HR (obese = -46 +/- 5; lean = -55 +/- 4 beats/min), and MAP (obese = -13 +/- 6; lean = -10 +/- 1 mmHg) similarly in lean and obese Zucker rats. The results indicate that the cardiovascular and metabolic responses to fasting and thermoneutrality are conserved in Zucker rats and suggest that intact leptin signaling may not be requisite for the metabolic and cardiovascular responses to reduced energy intake.

Animals↗

Central leptin infusion attenuates the cardiovascular and metabolic effects of fasting in rats.

The role of reduced leptin signaling in the regulation of cardiovascular responses to negative energy balance is not known. We tested the hypothesis that central infusion of leptin would attenuate the cardiovascular and metabolic responses to fasting. Male Sprague-Dawley rats, instrumented with telemetry devices and intracerebroventricular cannulas, were housed in metabolic chambers for continuous (24 hours) measurement of dark-phase (active) and light-phase (inactive) mean arterial pressure, heart rate, oxygen consumption, and respiratory quotient. Rats received central infusions of either saline (0.5 microL/h) or leptin (42 ng/h) for 6 days through osmotic pumps and were either fed ad libitum or were fasted for 48 hours followed by refeeding for 4 days. In ad lib animals, continuous intracerebroventricular leptin infusion significantly reduced caloric intake, body weight, and respiratory quotient compared with saline controls while having no effect on mean arterial pressure or heart rate. Fasting reduced mean arterial pressure, heart rate, oxygen consumption, and respiratory quotient in rats receiving saline infusions. Fasting-induced reductions in mean arterial pressure were specific to the active phase and were not attenuated by central leptin infusion. In contrast, intracerebroventricular leptin, at a dose that had no cardiovascular effects in ad lib control animals, completely prevented fasting-induced decreases in light-phase heart rate and oxygen consumption and blunted fasting-induced reductions in dark-phase heart rate and oxygen consumption. The results are consistent with the hypothesis that reductions in central leptin signaling contribute to the integrated cardiovascular and metabolic responses to acute caloric deprivation.

Animals↗

A sport-physiological perspective on bird migration: evidence for flight-induced muscle damage.

Exercise-induced muscle damage is a well-described consequence of strenuous exercise, but its potential importance in the evolution of animal activity patterns is unknown. We used plasma creatine kinase (CK) activity as an indicator of muscle damage to investigate whether the high intensity, long-duration flights of two migratory shorebird species cause muscle damage that must be repaired during stopover. In two years of study, plasma CK activity was significantly higher in migrating western sandpipers (a non-synchronous, short-hop migrant), than in non-migrants. Similarly, in the bar-tailed godwit (a synchronous, long-jump migrant), plasma CK activity was highest immediately after arrival from a 4000-5000km flight from West Africa to The Netherlands, and declined before departure for the arctic breeding areas. Late-arriving godwits had higher plasma CK activity than birds that had been at the stopover site longer. Juvenile western sandpipers making their first southward migration had higher plasma CK activity than adults. These results indicate that muscle damage occurs during migration, and that it is exacerbated in young, relatively untrained birds. However, the magnitude of the increases in plasma CK activity associated with migratory flight were relatively small, suggesting that the level of muscle damage is moderate. Migrants may avoid damage behaviourally, or have efficient biochemical and physiological defences against muscle injury.

Aging↗

Retinal arteriovenous communication.

BACKGROUND: Disturbances in development of the embryonic vascular system, though uncommon, may cause formation of retinal arteriovenous communications (RAC). Such anomalies may also involve the intracranial, orbital, and maxillofacial blood vessels. Field loss, neovascular glaucoma, optic atrophy, Parinaud syndrome, hemiparesis, hemiplegia, and proptosis may be associated with RAC. CASE REPORT: A 27-year-old woman was referred for photography of a vascular anomaly in her left eye. I noted a large arteriovenous malformation joining major temporal branches of the left central retinal artery and vein. External and internal examination of both eyes was otherwise unremarkable. Visual-field testing revealed nasal field disturbances for the left eye, but none for the right eye. CT scan showed no obvious intracranial abnormalities. CONCLUSIONS: Visual-field testing may show scotomas associated with retinal arteriovenous communications. It is possible for patients with RAC to have no associated vascular abnormalities elsewhere in the circulation of the head.

Adult↗

Nitric oxide-dependent modification of the sarcoplasmic reticulum Ca-ATPase: localization of cysteine target sites.

Skeletal muscle contraction and relaxation is modulated through the reaction of sarcoplasmic reticulum (SR) protein thiols with reactive oxygen and nitrogen species. Here, we have utilized high-performance liquid chromatography-electrospray mass spectrometry and a specific thiol-labeling procedure to identify and quantify cysteine residues of the SR Ca-ATPase that are modified by exposure to nitric oxide (NO). NO and/or NO-derived species inactivate the SR Ca-ATPase and modify a broad spectrum of cysteine residues with highest reactivities towards Cys364, Cys670, and Cys471. The selectivity of NO and NO-derived species towards the SR Ca-ATPase thiols is different from that of peroxynitrite. The efficiency of NO at thiol modification is significantly higher compared with that of peroxynitrite. Hence, NO has the potential to modulate muscle contraction through chemical reaction with the SR Ca-ATPase in vivo.

Animals↗

Modulation of lipogenic enzymes, fatty acid synthase and delta9-desaturase, in relation to migration in the western sandpiper (Calidris mauri).

Long-distance migration in birds is characterized physiologically by periods of rapid fattening and lipogenesis, and increased desaturation of fatty acids stored in adipose tissue. We investigated seasonal, age- and sex-related differences in activities of two lipogenic enzymes, fatty acid synthase and delta9-desaturase, in relation to migration in the small, Arctic-nesting western sandpiper (Calidris mauri). Migration, and associated lipogenesis and fattening, involved marked upregulation of these enzymes in this species. However, this increase in enzyme activity was only seen in actively migrating birds during spring migration, when fatty acid synthase and delta9-desaturase levels increased by 53% and 113%, respectively, compared to non-migrating birds. There was no change in fatty acid synthase enzyme activity during the premigration period, even though body mass of adult birds increased significantly during this period. Similarly, there was no increase in delta9-desaturase activity during premigration, despite the fact that birds increase the proportion of monounsaturated fatty acids in their fat stores at this time. We suggest that upregulation of lipogenic enzymes is required to support high rates of mass gain (0.4 g day(-1)) during short (1-4 day) periods at stop-over sites. However, slower rates of mass gain (0.09 g day(-1)) over several weeks prior to migration can be achieved without any increase in tissue-specific enzyme activity.

Adipose Tissue↗

Identification of three protein targets for reactive metabolites of bromobenzene in rat liver cytosol.

The hepatotoxicity of bromobenzene and many other simple organic chemicals is believed to be associated with covalent binding of chemically reactive metabolites to cellular proteins. Recently, a rat liver microsomal esterase was shown to be targeted by bromobenzene metabolites formed in vitro [Rombach, E. M., and Hanzlik, R. P. (1998) Chem. Res. Toxicol. 11, 178-184]. To identify protein targets for bromobenzene metabolites in cytosol, we incubated liver microsomes and glutathione-depleted liver cytosol from phenobarbital-treated rats with [(14)C]bromobenzene in vitro. In a separate experiment, we intraperitoneally injected a hepatotoxic dose of [(14)C]bromobenzene to phenobarbital-treated rats. The cytosol fractions from both experiments were recovered and analyzed for protein-bound radioactivity. Under the conditions that were used, 2.6 and 3.9 nmolar equiv of bromobenzene/mg of cytosolic protein was bound in vitro and in vivo, respectively. Denaturing polyacrylamide gel electrophoresis of these cytosolic proteins followed by phosphor imaging analysis revealed several radiolabeled protein bands over a broad molecular mass range, the patterns observed in vitro and in vivo being generally similar to each other. Cytosolic proteins labeled in vitro were separated by ion exchange chromatography and electrophoresis, and three major radioactive bands with estimated molecular masses of ca. 14, 25, and 30 kDa were in-gel digested with trypsin, followed by on-line HPLC electrospray ionization mass spectrometry of the resulting peptide mixtures. For the three protein bands, the observed peptide masses were found to match the predicted tryptic fragments of liver fatty acid binding protein, glutathione transferase subunit A1, and carbonic anhydrase isoform III, respectively, with 83, 45, and 59% coverage of the corresponding complete sequences. The possible relationship of the adduction of these proteins to the toxicological outcome is discussed.

Amino Acid Sequence↗

Concurrent reductions in blood pressure and metabolic rate during fasting in the unrestrained SHR.

Fasting produces multiple cardiovascular, metabolic, and behavioral responses. To examine the interrelationship between these responses, male spontaneously hypertensive rats (SHR; n = 8) implanted with cardiovascular telemetry devices were housed in metabolic chambers at 23 degrees C for 22-h daily measurements of physiological variables. The experimental apparatus was designed so that ingestive behavior was detected by photobeams and locomotion was detected by a load sensor. Cardiovascular and metabolic status were determined as both a function of the circadian cycle (12-h dark and 10-h light), as well as during periods of inactivity (no ingestion and minimal locomotion) within the dark and light phases. Data were obtained during baseline, 48-h of caloric deprivation, and 6 days of refeeding. Fasting produced significant reductions in mean arterial pressure (dark: -9.2+/-1.3 from 143.7+/-3.7 mm Hg; light: -8.6+/-1.8 from 140.1+/-3.7 mm Hg), heart rate (dark: -43.4+/-5.2 from 330.0+/-5.2 beats/min; light: -27.4+/-5.2 from 294.0+/-5.2 beats/min), and oxygen consumption (dark: -5.0+/-0.6 from 20.6+/-0.3 ml x min(-1) x kg (0.75); light: -2.7+/-0.2 from 14.9 +/-0.2 ml x min(-1) x kg(0.75)). Analysis of inactive periods during both light and dark phases revealed that these reductions were not dependent on behavioral effects. We conclude that fasting produces concurrent and interrelated reductions in cardiovascular and metabolic function in the SHR. The merging of cardiovascular telemetry, indirect calorimetry, and behavioral monitoring provides a powerful approach for investigation of the integrative physiological responses to energetic challenges.

Animals↗

Cardiovascular and metabolic responses of hypertensive and normotensive rats to one week of cold exposure.

Challenges to energy homeostasis, such as cold exposure, can have consequences for both metabolic and cardiovascular functioning. We hypothesized that 1-wk cold exposure (4 degrees C) would produce concurrent increases in metabolic rate (VO(2); indirect calorimetry), heart rate (HR), and mean arterial blood pressure (MAP) measured by telemetry. In the initial hours of change in ambient temperature (T(a)), both spontaneously hypertensive rats (SHRs) and normotensive Sprague-Dawley rats showed rapid increases (in cold) or decreases (in rewarming) of VO(2), HR, and MAP, although the initial changes in MAP and HR were more exaggerated in SHRs. Throughout cold exposure, HR, VO(2), food intake, and locomotor activity remained elevated but MAP decreased in both strains, particularly in the SHR. During rewarming, all measures normalized quickly in both strains except MAP, which fell below baseline (hypotension) for the first few days. The results indicate that variations of T(a) produce rapid changes in a suite of cardiovascular and behavioral responses that have many similarities in hypertensive and normotensive strains of rats. The findings are consistent with the general concept that the cardiovascular responses to cold exposure in rats are closely related to and perhaps a secondary consequence of the mechanisms responsible for increasing heat production.

Acclimatization↗

Peroxynitrite modification of protein thiols: oxidation, nitrosylation, and S-glutathiolation of functionally important cysteine residue(s) in the sarcoplasmic reticulum Ca-ATPase.

Skeletal muscle contraction and relaxation is efficiently modulated through the reaction of reactive oxygen-nitrogen species with sarcoplasmic reticulum protein thiols in vivo. However, the exact locations of functionally important modifications are at present unknown. Here, we determine by HPLC-MS that the modification of one (out of 24) Cys residue of the sarcoplasmic reticulum (SR) Ca-ATPase isoform SERCA1, Cys(349), by peroxynitrite is sufficient for the modulation of enzyme activity. Despite the size and nature of the SR Ca-ATPase, a 110 kDa membrane protein, identification and quantitation of Cys modification was achieved through labeling with 4-(dimethylamino)phenylazophenyl-4'-maleimide (DABMI) and/or N-(2-iodoethyl)trifluoroacetamide (IE-TFA) followed by an exhaustive tryptic digestion and on-line HPLC-UV-electrospray MS analysis. The reaction with IE-TFA generates aminoethylcysteine, a new trypsin cleavage site, which allows the production of specific peptide fragments that are diagnostic for IE-TFA labeling, conveniently identified by mass spectrometry. Exposure of the SR Ca-ATPase to low concentrations (0.1 mM) of peroxynitrite resulted in the fully reversible chemical modification of Cys at positions 344, 349, 471, 498, 525, and 614 (nitrosylation of Cys(344) and Cys(349) was seen), whereas higher concentrations of peroxynitrite (0.45 mM) additionally affected Cys residues at positions 636, 670, and 674. When the SR Ca-ATPase was exposed to 0.45 mM peroxynitrite in the presence of 5.0 mM glutathione (GSH), thiol modification became partially reversible and S-glutathiolation was detected for Cys residues at positions 344, 349, 364, 498, 525, and 614. The extent of enzyme inactivation (determined previously) quantitatively correlated with the loss of labeling efficiency (i) of a single Cys residue and (ii) of the tryptic fragment containing both Cys(344) and Cys(349). Earlier results had shown that the independent selective modification of Cys(344) is functionally insignificant [Kawakita, M., and Yamashita, T. (1987) J. Biochem. (Tokyo) 102, 103-109]. Thus, we conclude that modification of only Cys(349) is responsible for the modulation of the SR Ca-ATPase activity by peroxynitrite.

Acetamides↗

A novel trisaccharide glycolipid biosurfactant containing trehalose bears ester-linked hexanoate, succinate, and acyloxyacyl moieties: NMR and MS characterization of the underivatized structure.

A Gram-positive actinomycete growing on n-hexadecane secreted a family of anionic glycolipid surfactant homologs. The major homolog, with a molecular weight of 1210.6347, had the formula C58H98O26. Following mild alkaline saponification, 1H and 13C NMR spectroscopy were used to characterize the non-reducing trisaccharide backbone: beta-Glcp-(1-->3)-alpha-Glcp-(1<-->1)-alpha-Glcp ('laminaratrehalose'). Hexanoate, succinate, 3-hydroxyoctanoate, and 3-hydroxydecanoate were found in 3:1:1:1 molar ratio using GC-EIMS analysis of fatty acid methyl esters (FAME) prepared by transesterification. We found that the beta-hydroxy acids bore secondary hexanoate chains in 3-O-ester linkage, giving acyloxyacyl anions of appropriate m/z in FABMS and FABMS/MS spectra. COSY, HETCOR, HMBC, and HMQC NMR experiments established the acylation pattern: succinate at C-2 of the terminal alpha-glucopyranose ring; hexanoate at C-3" of the beta-glucopyranose ring; 3-hexanoyloxyoctanoate and 3-hexanoyloxydecanoate at the 2'- and 4-positions. In FABMS spectra, the homologs flanked the molecular ion by +/- 14 and +/- 28 amu, suggesting heterogeneity in acyl chain length.

Acylation↗

Protein modification during biological aging: selective tyrosine nitration of the SERCA2a isoform of the sarcoplasmic reticulum Ca2+-ATPase in skeletal muscle.

The accumulation of covalently modified proteins is an important hallmark of biological aging, but relatively few studies have addressed the detailed molecular-chemical changes and processes responsible for the modification of specific protein targets. Recently, Narayanan et al. [Narayanan, Jones, Xu and Yu (1996) Am. J. Physiol. 271, C1032-C1040] reported that the effects of aging on skeletal-muscle function are muscle-specific, with a significant age-dependent change in ATP-supported Ca2+-uptake activity for slow-twitch but not for fast-twitch muscle. Here we have characterized in detail the age-dependent functional and chemical modifications of the rat skeletal-muscle sarcoplasmic-reticulum (SR) Ca2+-ATPase isoforms SERCA1 and SERCA2a from fast-twitch and slow-twitch muscle respectively. We find a significant age-dependent loss in the Ca2+-ATPase activity (26% relative to Ca2+-ATPase content) and Ca2+-uptake rate specifically in SR isolated from predominantly slow-twitch, but not from fast-twitch, muscles. Western immunoblotting and amino acid analysis demonstrate that, selectively, the SERCA2a isoform progressively accumulates a significant amount of nitrotyrosine with age (approximately 3.5+/-0. 7 mol/mol of SR Ca2+-ATPase). Both Ca2+-ATPase isoforms suffer an age-dependent loss of reduced cysteine which is, however, functionally insignificant. In vitro, the incubation of fast- and slow-twitch muscle SR with peroxynitrite (ONOO-) (but not NO/O2) results in the selective nitration only of the SERCA2a, suggesting that ONOO- may be the source of the nitrating agent in vivo. A correlation of the SR Ca2+-ATPase activity and covalent protein modifications in vitro and in vivo suggests that tyrosine nitration may affect the Ca2+-ATPase activity. By means of partial and complete proteolytic digestion of purified SERCA2a with trypsin or Staphylococcus aureus V8 protease, followed by Western-blot, amino acid and HPLC-electrospray-MS (ESI-MS) analysis, we localized a large part of the age-dependent tyrosine nitration to the sequence Tyr294-Tyr295 in the M4-M8 transmembrane domain of the SERCA2a, close to sites essential for Ca2+ translocation.

Aging↗

Repair of oxidized calmodulin by methionine sulfoxide reductase restores ability to activate the plasma membrane Ca-ATPase.

We have investigated the ability of methionine sulfoxide reductase (MsrA) to maintain optimal calmodulin (CaM) function through the repair of oxidized methionines, which have been shown to accumulate within CaM in senescent brain [Gao, J., Yin, D. H., Yao, Y., Williams, T. D., and Squier, T. C. (1998) Biochemistry 37, 9536-9548]. Oxidatively modified calmodulin (CaMox) isolated from senescent brain or obtained by in vitro oxidation was incubated with MsrA. This treatment restores the functional ability of CaMox to activate the plasma membrane (PM) Ca-ATPase, confirming that (i) the decreased ability of CaM isolated from senescent animals to activate the PM Ca-ATPase results solely from methionine sulfoxide formation and (ii) MsrA can repair methionine sulfoxides within cytosolic proteins. We have used electrospray ionization mass spectrometry to investigate the extent and rates of methionine sulfoxide repair within CaMox. Upon exhaustive repair by MsrA, there remains a distribution of methionine sulfoxides within functionally reactivated CaMox, which varies from three to eight methionine sulfoxides. The rates of repair of methionine sulfoxides within individual tryptic fragments of CaMox vary by a factor of 2, where methionine sulfoxides located within hydrophobic sequences are repaired in preference to methionines that are more solvent accessible within the native structure. However, no single methionine sulfoxide is completely repaired in all CaM oxiforms. Decreases in the alpha-helical content and a disruption of the tertiary structure of CaM have previously been shown to result from methionine oxidation. Repair of selected methionine sulfoxides in CaMox by MsrA results in a partial refolding of the secondary structure, suggesting that MsrA repairs methionine sulfoxides within unfolded sequences until native-like structure and function are re-attained. The ability of CaMox isolated from senescent brain to fully activate the PM Ca-ATPase following repair by MsrA suggests the specific activity of MsrA is insufficient to maintain CaM function in aging brain. These results are discussed in terms of the possible regulatory role MsrA may play in the modulation of CaM function and calcium homeostasis under conditions of oxidative stress.

Aging↗

Validation of immunotoxicology techniques in passerine chicks exposed to Oil Sands tailings water.

Avian species, through their trophic relationships, may represent ideal indicators for assessing environmental health. In this study several assays of immune function in young passerines are validated and compared. From 6 to 10 days of age, zebra finch nestlings (Taeniopygia guttata) were given daily oral doses of Oil Sands tailings water (CT), an immunosuppressant dexamethasone, or phosphate-buffered saline. At 9-10 days of age, a phytohemagglutinin (PHA) skin test of immune function was conducted; at 11 days of age, five chicks from each group were euthanized for gross and histopathologic examination of immune system organs. The remaining birds were vaccinated with sheep red blood cells (srbc) to evaluate antibody-mediated immunity. The main findings were that in 10-day-old nestlings, T lymphocytes were sensitive to PHA stimulation, while B lymphocytes were unable to respond to srbc; that hematocrit was approximately 30% lower than in mature birds; that precision of leucocrit determination was heavily technique-dependent; that endogenous steroids increased the total leucocrit, while exogenous steroids increased heterophil and decreased lymphocyte counts, thus increasing H:L; that dexamethasone exposure temporarily reduced growth rate; that CT exposure stimulated germinal cell development in the bursa of Fabricius; and that dexamethazone and CT exposure were associated with decreased splenic white pulp formation.

Animals↗

Parental and first generation effects of exogenous 17beta-estradiol on reproductive performance of female zebra finches (Taeniopygia guttata).

Steroids hormones have numerous "activational" effects in adult birds, regulating sexual behavior, and more recently maternal androgens have been shown to have potentially important "organizational" effects in ovo, influencing offspring growth, development, and behavior. In this study I investigated parental and first-generation effects of exogenous estrogens on female reproduction in zebra finches (Taeniopygia guttata). 17beta-Estradiol (E2; 1.2 microg/g, 4 daily injections i.m.) elevated plasma levels of the yolk precursors, vitellogenin (VTG) and very low-density lipoprotein (VLDL), in nonbreeding females to levels similar to those of breeding females. However, E2-treatment of breeding females caused no significant change in plasma VTG or VLDL levels compared to control birds (measured at the 1-egg stage), and there was no difference in reproductive performance between groups (egg size, clutch size, timing of laying). E2-treated females produced significantly more daughters than sons (21F:8M) at fledging, compared to control females (18F:19M). Nestling mortality was significantly higher in broods of E2-treated females, suggesting that the skewed sex ratio may have resulted from differential mortality of male chicks. The pattern of chick mortality in E2-broods was not consistent with this being caused by estrogen-mediated changes in parental behavior (e.g., provisoning). Mean egg mass of daughters of E2-treated females was typical of experienced, adult breeders, and larger than normal, first-time breeders or control offspring (0.947 vs 0.850 g). There was no treatment effect on offspring clutch size or laying interval. These results suggest that early exposure to maternal estrogens in ovo might be involved in establishing intraindividual variation in female-specific phenotypic traits, as has previously been demonstrated for androgens and male behavioral traits (e.g., aggression).

Animals↗

Carboxylase genes of Sulfolobus metallicus.

Carbon dioxide limitation of Sulfolobus metallicus resulted in increased cellular concentrations of polypeptides that were predicted to be biotin carboxylase and biotin carboxyl-carrier-protein components of a protein complex. These polypeptides were coeluted from a native polyacrylamide gel and were estimated at 19 and 59 kDa after separation by denaturing gel electrophoresis. Their encoding genes were identified, sequenced and shown to code for polypeptides of 18,580 and 58,235 Da with similarities to biotin carboxyl carrier proteins and biotin carboxylases, respectively. The genes overlapped at the second of two stop codons that terminated the carboxylase gene. A third gene occurred on the opposite strand, 293 bp upstream of the biotin carboxylase gene. Its deduced amino acid sequence was similar to those of carboxyl transferase subunits of carboxylase enzymes, in particular to those of the propionyl-CoA carboxylases. It is proposed that the three described genes could encode the key enzyme complex responsible for carbon dioxide fixation during autotrophic growth of the thermoacidophilic archaea.

Acetyl-CoA Carboxylase↗