Trophic determinants of hypopus induction in the stored-product mite Lepidoglyphus destructor (Acari: Astigmata)

A unique (synapomorphic) characteristic of astigmatic mites is the heteromorphic deuteronymph also called hypopus. It is a non-feeding and facultative instar between protonymph and tritonymph. The hypopus is adapted for dispersal and sometimes also for dormancy, as in Lepidoglyphus destructor. The experiments reveal a correlation between the composition of the foodstuff, the duration of development of homomorphic instars, the mortality of protonymphs and the production of hypopodes. As food quality decreases, development lasts longer, mortality increases and hypopodes are produced in greater numbers. Disadvantageous trophic conditions of varied chemical nature favour the induction of hypopodes. The experimental data show that hypopus incidences (as percentage individuals of a population) depend on the relative proportions of constituents of an ingested foodstuff. What matters is the ratio between nourishing foodstuff components and those that are of little or no nutritional value. When a certain ratio does not meet a presumed metabolically required level of nutrients a nutritional deficiency results and hypopus induction is triggered, provided that adequate genetic propensities for hypopus production are present (L. destructor is highly polymorphic for hypopus production). Specific key substances are apparently not involved, and composite properties of a foodstuff are crucial for hypopus induction. Decrease of food quality (not poor food per se) during the hypopus-inducible period (late larval to early protonymphal phase) promotes hypopus induction. The interpretation matches the ecological scene. When trophic deterioration of a patch habitat sets in, often as a result of overcrowding, conditions will eventually become untenable. As a response to incurring nutritional deficiencies the mites will induce hypopodes, which provide for escape from or survival at the decaying habitat patch. Experiments support the threshold model of quantitative genetics for hypopus expression as previously inferred from other experiments with L. destructor.     

Genetic and environmental determinants of menstrual characteristics

BACKGROUND:

The impact of women''s menstrual cycle on her quality of life, health, work, and community is substantial. Menstrual disturbance is linked with general ill conditions such as migraine, asthma, and endocrinopathies. The clinical significance of medical interventions to prevent these conditions becomes clear if the role of genetic or environment is clarified.

AIMS:

To identify the genetic and environmental contribution on menstrual characteristics.

SETTING AND DESIGN:

This was a cross-sectional study in 2 Asian countries.

MATERIALS AND METHODS:

2 cohorts of monozygotic and dizygotic twins born between (1945-1988, n = 122) and (1951-1993, n = 71) were taken. A standard questionnaire was designed inclusive of socio- demographic characteristics of subjects as well as menstrual history (duration, interval, amount, irregularity). Subjects were interviewed by phone.

STATISTICAL ANALYSIS:

Quantitative variables were analyzed using Falconars’ formula as well as maximum likelihood analysis. Structural modeling was then applied to twin correlations to provide estimates of the relative genetic and/or environmental factors contribution in determining the measured trait.

RESULTS:

Menstrual characteristics were found to be under environmental influence where the best fitting model for menstrual interval and duration was common environment. CDF plotting confirmed the results for both variables. Proband-wise concordance analysis for amount of menstruation, amenorrhea, and irregular menstruation revealed no genetic influence. The best fitting model for menstrual irregularity was CE (C73%, E27%). The same model was defined for amenorrhea (C48%, E52%).

CONCLUSIONS:

Environmental factors are most likely responsible to determine the menstrual flow, its integrity, and regularity. These factors need to be studied further.     

Genetic and environmental determinants of skin color

Skin reflectance measurements on a sample of 154 Black and 191 White same-sex twin pairs, attending Philadelphia area schools, are analyzed to determine the effects of genetic and environmental factors. The measurements obtained in July and August, on the forehead, inner upper arm, and flexor surface of the forearm with red, green, and blue filters, were reduced to one index which we call skin color. Analysis of this index using the path analysis of Rao et al. ('74) estimates the major variance components due to racial, residual genetic, and common environmental factors as 67%, 5%, and 22%, respectively.     

Genetic and environmental determinants of malaria parasite virulence in mosquitoes

Models of malaria epidemiology and evolution are frequently based on the assumption that vector-parasitic associations are benign. Implicit in this assumption is the supposition that all Plasmodium parasites have an equal and neutral effect on vector survival, and thus that there is no parasite genetic variation for vector virulence. While some data support the assumption of avirulence, there has been no examination of the impact of parasite genetic diversity. We conducted a laboratory study with the rodent malaria parasite, Plasmodium chabaudi and the vector, Anopheles stephensi, to determine whether mosquito mortality varied with parasite genotype (CR and ER clones), infection diversity (single versus mixed genotype) and nutrient availability. Vector mortality varied significantly between parasite genotypes, but the rank order of virulence depended on environmental conditions. In standard conditions, mixed genotype infections were the most virulent but when glucose water was limited, mortality was highest in mosquitoes infected with CR. These genotype-by-environment interactions were repeatable across two experiments and could not be explained by variation in anaemia, gametocytaemia, blood meal size, mosquito body size, infection rate or oocyst burden. Variation in the genetic and environmental determinants of virulence may explain conflicting accounts of Plasmodium pathogenicity to mosquitoes in the malaria literature.     

Genetic, behavioral and environmental determinants of male longevity in Caenorhabditis elegans

Males of the nematode Caenorhabditis elegans are shorter lived than hermaphrodites when maintained in single-sex groups. We observed that groups of young males form clumps and that solitary males live longer, indicating that male-male interactions reduce life span. By contrast, grouped or isolated hermaphrodites exhibited the same longevity. In one wild isolate of C. elegans, AB2, there was evidence of copulation between males. Nine uncoordinated (unc) mutations were used to block clumping behavior. These mutations had little effect on hermaphrodite life span in most cases, yet many increased male longevity even beyond that of solitary wild-type males. In one case, the neuronal function mutant unc-64(e246), hermaphrodite life span was also increased by up to 60%. The longevity of unc-4(e120), unc-13(e51), and unc-32(e189) males exceeded that of hermaphrodites by 70-120%. This difference appears to reflect a difference in sex-specific life span potential revealed in the absence of male behavior that is detrimental to survival. The greater longevity of males appears not to be affected by daf-2, but is influenced by daf-16. In the absence of male-male interactions, median (but not maximum) male life span was variable. This variability was reduced when dead bacteria were used as food. Maintenance on dead bacteria extended both male and hermaphrodite longevity.     

Genetic and environmental determinants of dental occlusal variation in twins of different nationalities

We have compared 10 occlusal traits in 358 monozygous and dizygous twin pairs in 4 different samples and estimated genetic variances for these features. Variable and frequently nonsignificant genetic variance was noted across samples for incisal overbite and overjet, sagittal molar relationship, posterior crossbite, and rotations and displacements of anterior teeth. Heritability estimates (when appropriately calculated) were low in magnitude (0-40%) and erratic, emphasizing the importance of environmental influences on occlusal variation and the variability of apparent genetic determinants with respect to the environment or population in which they are measured.     

Genetic variability and ecological adaptability of hypopus formation in a stored product mite

Occurrence inLepidoglyphus destructor of a facultative developmental stage (hypopus) adapted for dispersal and dormancy depends on genotype x environment interaction. Dietary factors affect hypopus formation, but the response of individuals to food quality greatly differs according to genotype. Large genetic variation in the control of hypopus formation exists within as well as between populations. Response to selection is rapid and reversible. The trait has substantial potential for selective adaptation to unpredictably varying environments and for evolutionary change.     

Genetic and environmental determinants of interferon-tau secretion by in vivo- and in vitro-derived bovine blastocysts

Several experiments were conducted to assess the effects of genotype and various culture media on interferon-tau secretion by in vitro-derived bovine blastocysts and to compare these values with interferon released by blastocysts flushed from superovulated cows. In experiment 1, oocytes were inseminated with semen from three different bulls. While paternal genotype had no effect on cleavage rate, the size or hatching ability of blastocysts, it was a significant determinant of the embryo's ability to develop to the blastocyst stage and of subsequent interferon-tau secretion. In the second experiment, embryos were cultured in synthetic oviductal fluid containing either polyvinyl alcohol, bovine serum albumin or fetal bovine serum. While there was no effect of supplement on the percentage of embryos developing to the blastocyst stage, blastocysts which formed in medium with polyvinyl alcohol had significantly fewer cells, were older at blastocyst formation and produced significantly more interferon-tau. In the third experiment, embryos were cultured to the blastocyst stage in either TCM199 alone or in co-culture with buffalo rat liver, bovine oviductal or bovine uterine epithelial cells. Culture with oviductal or buffalo rat liver cells increased blastocyst cell number, although secretion of interferon-tau was not affected. In the final experiment, bovine blastocysts were flushed from superovulated cows on Day 7 following insemination. Overall, secretion of interferon-tau by in vivo-produced blastocysts did not differ from that of age-matched blastocysts produced in vitro.     

Genetic determinants of aggression and impulsivity in humans

Human aggression/impulsivity-related traits have a complex background that is greatly influenced by genetic and non-genetic factors. The relationship between aggression and anxiety is regulated by highly conserved brain regions including amygdala, which controls neural circuits triggering defensive, aggressive, or avoidant behavioral models. The dysfunction of neural circuits responsible for emotional control was shown to represent an etiological factor of violent behavior. In addition to the amygdala, these circuits also involve the anterior cingulated cortex and regions of the prefrontal cortex. Excessive reactivity in the amygdala coupled with inadequate prefrontal regulation serves to increase the likelihood of aggressive behavior. Developmental alterations in prefrontal-subcortical circuitry as well as neuromodulatory and hormonal abnormality appear to play a role. Imbalance in testosterone/serotonin and testosterone/cortisol ratios (e.g., increased testosterone levels and reduced cortisol levels) increases the propensity toward aggression because of reduced activation of the neural circuitry of impulse control and self-regulation. Serotonin facilitates prefrontal inhibition, and thus insufficient serotonergic activity can enhance aggression. Genetic predisposition to aggression appears to be deeply affected by the polymorphic genetic variants of the serotoninergic system that influences serotonin levels in the central and peripheral nervous system, biological effects of this hormone, and rate of serotonin production, synaptic release and degradation. Among these variants, functional polymorphisms in the monoamine oxidase A (MAOA) and serotonin transporter (5-HTT) may be of particular importance due to the relationship between these polymorphic variants and anatomical changes in the limbic system of aggressive people. Furthermore, functional variants of MAOA and 5-HTT are capable of mediating the influence of environmental factors on aggression-related traits. In this review, we consider genetic determinants of human aggression, with special emphasis on genes involved in serotonin and dopamine metabolism and function.     

Genetic determinants of cancer metastasis

Metastasis can be viewed as an evolutionary process, culminating in the prevalence of rare tumour cells that overcame stringent physiological barriers as they separated from their original environment and developmental fate. This phenomenon brings into focus long-standing questions about the stage at which cancer cells acquire metastatic abilities, the relationship of metastatic cells to their tumour of origin, the basis for metastatic tissue tropism, the nature of metastasis predisposition factors and, importantly, the identity of genes that mediate these processes. With knowledge cemented in decades of research into tumour-initiating events, current experimental and conceptual models are beginning to address the genetic basis for cancer colonization of distant organs.     

Genetic analysis and screening of pyrethroid resistance mutations in Varroa destructor populations from Turkey

Experimental and Applied Acarology - Varroa destructor is the most common ectoparasite of the Western honey bee (Apis mellifera L.) worldwide and poses a serious threat to bee health. Synthetic...     

Respiratory and metabolic responses of the Australian Yabby Cherax destructor to progressive and sustained environmental hypoxia

The Australian Yabby, Cherax destructor, inhabits occasionally hypoxic water. The respiratory gas, acid-base, metabolite and energetic status of this crayfish was assessed during progressive hypoxia and during 3 h at a water PO₂ of 1.33 kPa. The O₂ affinity of haemocyanin from C. destructor was increased by lactate (Δlog P ₅₀/Δlog[lactate] = −0.111) and by Ca (Δlog P ₅₀/Δlog[Ca] = −0.62) but not by urate. While the non-bicarbonate buffering capacity was low (Δ[HCO₃ ⁻]/ ΔpH=−4.89) the haemocyanin had a low sensitivity to pH changes (ϕ = −0.33). The crayfish showed a compensatory hyperventilation, which induced a respiratory alkalosis, until the water O₂ partial pressure declined below 2.67 kPa, after which the O₂ uptake rate was approximately 10% of normoxic rates. The high haemocyanin-O₂ affinity maintained haemolymph O₂ content during progressive hypoxia despite the normally low arterial O₂ partial pressure of C. destructor. During severe hypoxia, pH decreased but increased lactate aided in maintaining haemocyanin-O₂ saturation. The importance of regulated haemocyanin-O₂ affinity in hypoxic C. destructor was reduced by lowered metabolism, including reduced cardiac output, and the consequent reduction in O₂ requirement. Anaerobiosis became important only at very low PO₂ but thereafter proceeded rapidly, supported by a marked hyperglycaemia. There was no depletion of adenylates, even after 3 h of severe hypoxia. The tail muscle of C. destructor held small amounts of glycogen which would sustain anaerobiosis for a only a few hours. Hypometabolism seems an important hypoxic response but severe hypoxia may encourage the crayfish to breathe air. Accepted: 26 February 1998     

Genetic determinants of antibiotic resistance in enterobacteria

Antibiotic resistance of enterobacterial strains from population isolated in Krasnodar region is rather often controlled by the "plasmid" genes. The conclusion is based on using the colony hybridization with [32P]-DNA fragments of plasmids, carrying the genetic determinants of antibiotic resistance, as a method for antibiotic resistance, genes screening. Kanamycin resistance in the majority of strains is coded by APH (3') II gene, streptomycin resistance by APH (3") gene, chloramphenicol resistance by CATI, sulphonilamide resistance by DHPS type II gene. Tetracycline resistance of the studied enterobacterial strains is not connected with the widespread genetic determinants of a new class tetracycline resistance.     

Genetic determinants of phenotypic diversity in humans

New technologies for rapidly assaying DNA sequences have revealed that the degree and nature of human genetic variation is far more complex then previously realized. These same technologies have also resulted in the identification of common genetic variants associated with more than 30 human diseases and traits.     

Genetic determinants of hepatic steatosis in man

Hepatic steatosis is one of the most common liver disorders in the general population. The main cause of hepatic steatosis is nonalcoholic fatty liver disease (NAFLD), representing the hepatic component of the metabolic syndrome, which is characterized by type 2 diabetes, obesity, and dyslipidemia. Insulin resistance and excess adiposity are considered to play key roles in the pathogenesis of NAFLD. Although the risk factors for NAFLD are well established, the genetic basis of hepatic steatosis is largely unknown. Here we review recent progress on genomic variants and their association with hepatic steatosis and discuss the potential impact of these genetic studies on clinical practice. Identifying the genetic determinants of hepatic steatosis will lead to a better understanding of the pathogenesis and progression of NAFLD.     

Genetic variation of sitting frequency and duration in pigs

Prior to weaning, many piglets die from crushing, chilling, starvation diarrhea and weakness. Piglets often die from crushing by the sow when she lies down after sitting. The objective of this study was to determine the amount of heritable genetic variation of sitting behavior. A total of 312 pigs from 62 litters were given ad libitum feed and water. Frequency and occurrence of sitting were summarized from 24-h video records. Heritability estimates (h²) were calculated for these traits using a full-sib analysis. The h² for the occurrence of sitting was 0.41 ± 0.14 and for frequency of sitting was 0.43 ± 0.14. Genetic correlation between frequency and occurrence of sitting was 0.84 and the phenotypic correlation was 0.68 (P < 0.01). Sitting behavior was moderately to highly heritable indicating possible favorable selection against occurrence of this trait. Genetic selection against sow sitting could potentially decrease mortality rates among piglets, increase production and decrease costs for pork producers.     

Genetic determinants of hyaloid and retinal vasculature in zebrafish

Background

The retinal vasculature is a capillary network of blood vessels that nourishes the inner retina of most mammals. Developmental abnormalities or microvascular complications in the retinal vasculature result in severe human eye diseases that lead to blindness. To exploit the advantages of zebrafish for genetic, developmental and pharmacological studies of retinal vasculature, we characterised the intraocular vasculature in zebrafish.

Results

We show a detailed morphological and developmental analysis of the retinal blood supply in zebrafish. Similar to the transient hyaloid vasculature in mammalian embryos, vessels are first found attached to the zebrafish lens at 2.5 days post fertilisation. These vessels progressively lose contact with the lens and by 30 days post fertilisation adhere to the inner limiting membrane of the juvenile retina. Ultrastructure analysis shows these vessels to exhibit distinctive hallmarks of mammalian retinal vasculature. For example, smooth muscle actin-expressing pericytes are ensheathed by the basal lamina of the blood vessel, and vesicle vacuolar organelles (VVO), subcellular mediators of vessel-retinal nourishment, are present. Finally, we identify 9 genes with cell membrane, extracellular matrix and unknown identity that are necessary for zebrafish hyaloid and retinal vasculature development.

Conclusion

Zebrafish have a retinal blood supply with a characteristic developmental and adult morphology. Abnormalities of these intraocular vessels are easily observed, enabling application of genetic and chemical approaches in zebrafish to identify molecular regulators of hyaloid and retinal vasculature in development and disease.