Hr Locus Research Articles

Peran Pelatihan SDM dan Locus of Control terhadap Kepuasan Kerja dan Implikasinya terhadap Produktivitas Kerja Aparatur Desa di Kabupaten Lebak

In order to effectively navigate the changing landscape of modern work, it is crucial for human resources to possess dependable, autonomous, and proficient skills in carrying out their primary responsibilities and functions as employees. This includes demonstrating a strong commitment and a strong work ethic that aligns with their job requirements, ultimately leading to optimal work productivity. Work productivity is a cognitive disposition that consistently enhances existing conditions. An enhanced conviction in one's ability to perform a task more effectively than previously. The objective of this study is to assess and examine the impact of HR training, locus of control, and job satisfaction on work productivity, as well as the impact of HR training and locus of control on job satisfaction. This study employs a quantitative descriptive research methodology. The descriptive approach in research seeks to quantify and measure existent phenomena. Quantitative data analysis is employed to compute the statistical outcomes of Structural Equation Modeling-Partial Least Square (SEM-PLS) with the objective of testing the hypothesis. The hypothesis test results indicate that HR training does not have a substantial impact on work productivity. However, Locus of Control has a notable beneficial influence on work productivity and job satisfaction. HR training does not have any impact on job satisfaction, while Locus of Control has a notable positive influence on job satisfaction. Additionally, it is seen that work productivity is significantly improved by HR training. The findings indicate that HR training does not have a discernible impact on productivity and work satisfaction. Work productivity is significantly enhanced by job happiness. The impact of Locus of Control on the productivity and job satisfaction of Village Officials in Lebak Regency is notably good.

Flowering time adaption in Swedish landrace pea (Pisum sativum L.).

BackgroundCultivated crops have repeatedly faced new climatic conditions while spreading from their site of origin. In Sweden, at the northernmost fringe of Europe, extreme conditions with temperature-limited growth seasons and long days require specific adaptation. Pea (Pisum sativum L.) has been cultivated in Sweden for millennia, allowing for adaptation to the local environmental conditions to develop. To study such adaptation, 15 Swedish pea landraces were chosen alongside nine European landraces, seven cultivars and three wild accessions. Number of days to flowering (DTF) and other traits were measured and the diversity of the flowering time genes HIGH RESPONSE TO PHOTOPERIOD (HR), LATE FLOWERING (LF) and STERILE NODES (SN) was assessed. Furthermore, the expression profiles of LF and SN were obtained.ResultsDTF was positively correlated with the length of growing season at the site of origin (GSO) of the Swedish landraces. Alleles at the HR locus were significantly associated with DTF with an average difference of 15.43 days between the two detected haplotypes. LF expression was found to have a significant effect on DTF when analysed on its own, but not when HR haplotype was added to the model. HR haplotype and GSO together explained the most of the detected variation in DTF (49.6 %).ConclusionsWe show local adaptation of DTF, primarily in the northernmost accessions, and links between genetic diversity and diversity in DTF. The links between GSO and genetic diversity of the genes are less clear-cut and flowering time adaptation seems to have a complex genetic background.Electronic supplementary materialThe online version of this article (doi:10.1186/s12863-016-0424-z) contains supplementary material, which is available to authorized users.

E Integrative genomics approaches identify new genes controlling heart rate

IntroductionHeart rate (HR) is a fundamental measure of cardiac function, and is of prognostic and therapeutic significance. We applied genetic and genomic approaches to identify new loci and genes controlling...

The flowering locus Hr colocalizes with a major QTL affecting winter frost tolerance in Pisum sativum L.

An understanding of the genetic determinism of frost tolerance is a prerequisite for the development of frost tolerant cultivars for cold northern areas. In legumes, it is not known to which extent vernalization requirement or photoperiod responsiveness are necessary for the development of frost tolerance. In pea (Pisum sativum L.) however, the flowering locus Hr is suspected to influence winter frost tolerance by delaying floral initiation until after the main winter freezing periods have passed. The objective of this study was to dissect the genetic determinism of frost tolerance in pea by QTL analysis and to assess the genetic linkage between winter frost tolerance and the Hr locus. A population of 164 recombinant inbred lines (RILs), derived from the cross Champagne x Terese was evaluated both in the greenhouse and in field conditions to characterize the photoperiod response from which the allele at the Hr locus was inferred. In addition, the population was also assessed for winter frost tolerance in 11 field conditions. Six QTL were detected, among which three were consistent among the different experimental conditions, confirming an oligogenic determinism of frost tolerance in pea. The Hr locus was found to be the peak marker for the highest explanatory QTL of this study. This result supports the hypothesis of the prominent part played by the photoperiod responsiveness in the determinism of frost tolerance for this species. The consistency of three QTL makes these positions interesting targets for marker-assisted selection.

Molecular basis for the rhino Yurlovo (hr(rhY)) phenotype: severe skin abnormalities and female reproductive defects associated with an insertion in the hairless gene.

In 1989, mice bearing mutations at the hr (hairless) locus were first proposed as a model for the human hair growth disorder papular atrichia, since in both these mice and in corresponding patients, a complete hair loss develops due to disintegration of the normal follicle structure into dermal cysts and so-called utriculi. Recently, the human hairless gene was characterized, and pathogenetic mutations were found to be associated with a recessively inherited form atrichia with papular lesions; however, the functions of hr gene remain unclear. Allelic mutations in the murine hairless gene represent a potentially powerful tool to elucidate the role of the hairless gene protein product in hair follicle physiology. In 1980, several naked animals were discovered in a breeding colony of B10.R109/Y mice maintained in the Laboratory of Experimental Biological Models (L.E.B.M., Yurlovo, Moscow District, Russia). By cross breeding with hairless HRS/J hr/hr mice, this mutation was shown to be allelic with hairless. Here, we describe the molecular basis of the hr(rhY) mutation in mice, which consists of a 13 bp insertion in exon 16 of the hr gene. Histological evaluation of Yurlovo mouse skin revealed some differences as compared to the hairless and rhino mutations, with the formation of dermal megacysts being the most specific peculiarity of the Yurlovo mutation. These results, together with previous studies of hr(rhY)/hr(rhY) mutant mice, suggest that the rhino Yurlovo (hr(rhY)) mutation represents a third and potentially more severe variation of the hairless phenotype.

Patterns of Hairless ( hr) Gene Expression in Mouse Hair Follicle Morphogenesis and Cycling

The hr (hairless) gene encodes a putative transcription factor with restricted expression in the skin and brain. Mutations in the hr locus cause papular atrichia in humans and complete hair loss in mice and other mammals. To further elucidate the role of hr in skin biology, and to identify potential target cells for hr regulation, we studied hr mRNA localization during hair follicle (HF) morphogenesis and cycling in normal C57BL/6J mice. In situ hybridization revealed that hr expression was present in the suprabasal cell layers of the epidermis, whereas the basal and highly differentiated keratinocytes of the granular layer were hr-negative. During the early stages of HF morphogenesis, hr mRNA was detected in the developing hair peg. Later, it became concentrated in the HF infundibulum, in the HF matrix, and in the inner root sheath (IRS), whereas the dermal papilla (DP) and outer root sheath were consistently hr mRNA-negative. During catagen, hr gene expression gradually declined in the regressing IRS, shortly but dramatically increased in the zone of developing club hair, and became up-regulated in the epithelial cells adjacent to the DP. The co-localization of hr mRNA with the site of the morphological defects in mutant skin implicates hr as a key factor in regulating basic cellular processes during catagen, including club hair formation, maintenance of DP-epithelial integrity, IRS disintegration, and keratinocyte apoptosis in the HF matrix.

The hairless gene of the mouse: relationship of phenotypic effects with expression profile and genotype.

Various mutations of the hairless (hr) gene of mice result in hair loss and other integument defects. To examine the role of the hr gene in mouse development, the expression profile of hr has been determined by in situ hybridisation and correlated to the nature of genetic changes and morphological abnormalities in different mutant animals. Four variant alleles have been characterised at the molecular level. hr/hr mice produce reduced, but significant, levels of hr mRNA whereas other alleles contain mutations which would be expected to preclude the synthesis of functional product, demonstrating a correlation between allelic variation at the hr locus and phenotypic severity. hr expression was shown to be widespread and temporally regulated. It was identified in novel tissues such as cartilage, developing tooth, inner ear, retina, and colon as well as in skin and brain. Analysis of mice homozygous for the rhino allele of hairless revealed that, although no morphological defects were detectable in many tissues normally expressing hr, previously undescribed abnormalities were present in several tissues including inner ear, retina, and colon. These findings indicate that the hairless gene product plays a wider role in development than previously suspected. Dev Dyn 1999;216:113-126.

Flowering genes and the photothermal flowering responses of pea (Pisum sativum): a re-analysis

Attempts to quantify the effects of the flowering genes Lf, Sn andHr in Pisum sativum L. on durations from sowing to flowering (f) have been hindered by the often strongly interactive effects of temperature and photoperiod. The original data of Berry and Aitken (Australian Journal of Plant Physiology 6, 573–587, 1979) for six cultivars have been re-analysed as rates of progress from sowing to flowering (1/f) and expressed as functions of mean pre-flowering values of temperature (T) and photo-period (P). The photothermal responses of rates of progress from sowing to flowering were clearly divided into two planes, with the boundary defined by the critical photoperiod (Pc). Variations in the response to temperature when P<Pc were associated with differences in alleles at the Lf locus, whereas variations when P>Pc were associated with differences at the Hr locus in the presence of Sn. Allele sn determined a single-plane response to temperature alone (i.e. a day-neutral response). The base temperature for 1/f when P>Pc was 1˚C for all six cultivars. The linear photothermal model used provided a robust quantitative basis for analysing the effect of flowering genes in pea.

Molecular basis of a novel rhino (hr(rhChr)) phenotype: a nonsense mutation in the mouse hairless gene.

The hairless and rhino mutations are autosomal recessive allelic mutations that map to mouse Chromosome 14. In general, the rhino phenotype is a more severe manifestation of the hairless phenotype. In both hairless and rhino mice, the hair begins shedding in a cephalocaudal pattern within 7 days after birth, and never regrows due to a series of irreversible cellular events. The hairless mutation closely resembles the human disease known as papular atrichia (MIM 209500). Recently, this disease was linked to Chromosome 8p12, the human homolog of hairless was cloned and mapped to the same locus, and mutations have been identified in several different families. In order to gain insight into the pathophysiology of disease in papular atrichia, we sought to utilize mouse mutations as in vivo model systems. In this study, we report the identification of a homozygous nonsense mutation in the coding region of the hr gene in a hairless mouse captured on a chicken farm in the Midwestern United States. To reflect the place of identification of this new mutation at the hr locus, we have designated this allele hr(rhChr) using the laboratory code Chr (Christiano).

Insertional mutation of the hairless locus on mouse Chromosome 14

Crosses between heterozygous transgenic mice from line 5053 produced offspring with progressive irreversible hair loss beginning at day 19. With increasing age, the skin of these animals became thicker and plicated in appearance. Histological analysis revealed the complete absence of normal hair follicles and numerous intradermic cystic structures, which enlarged with time and became filled with keratinaceous material. Test crosses demonstrated that the affected animals are homozygous for the transgene insertion. The clinical and histological phenotype of the new mutant closely resembles that of the rhino allele at the hairless locus on Chromosome (Chr) 14. Complementation tests and linkage analysis indicate that the transgene has interrupted the hairless locus. It has been demonstrated previously that mutation at the hr locus is accompanied by a variety of immune deficiencies. Many of the older affected transgenic mice developed an impetigo-like skin eruption which responded to antibiotic ointment and which may reflect impaired immune function. The transgenic allele, hrTgN5053Mm, will be useful for identification of the transcription unit of the hairless locus.

Genetic variation of iron-induced uroporphyria in mice

Iron overload causes inhibition of hepatic uroporphyrinogen decarboxylase (UROD) and uroporphyria in C57BL/10ScSn but not DBA/2 mice [Smith, Cabral, Carthew, Francis and Manson (1989) Int. J. Cancer 43, 492-496]. We have investigated the induction of uroporphyria in 12 inbred strains of mice 25 weeks after iron treatment (600 mg/kg) to determine if there was any correlation with the Ah locus. Under these conditions, inhibition of UROD occurred to varying degrees in Ahd mice (SWR and AKR) as well as nominally Ahb-1 (C57BL/6J, C57BL/10ScSn and C57BL/10-cc) and Ahb-2 strains (BALB/c and C3H/HeJ). Five other Ahb or Ahd strains (C57BL/Ks, A/J, CBA/J, LP and DBA/2) were unaffected. Thus there appeared to be no correlation with the Ah phenotype and this illustrated that some other variable inherited factors are involved. Comparisons between another susceptible strain, A2G, and the congenic A2G-hr/+strain (carrying the recessive hr gene) showed a modulating influence associated with the hr locus. In contrast with individual mice of inbred strains, which showed consistent responses to iron, those of the outbred MF1 strain showed a spectrum of sensitivities as might be expected for a heterogeneic stock. The rate of porphyria development was accelerated by administration of 5-aminolaevulinic acid (5-ALA) in the drinking water, but this did not overcome strain differences. Among four strains the order of susceptibility was SWR > C57BL/10ScSn > C57B1/6J > DBA/2 (the last strain was completely resistant). With degrees of iron loading greater than 600 mg of Fe/kg (1200-1800 mg of Fe/kg) C57BL/10ScSn mice (after 20 weeks) and SWR mice (after 5 weeks which included 4 weeks of 5-ALA treatment) had less inhibition of UROD and a lower uroporphyric response, showing that there was an optimum level of liver iron concentration. Studies on selected microsomal enzyme activities associated with cytochrome P-450 showed no correlation with the propensities of strains to develop porphyria. These activities included the NADPH-dependent oxidation of uroporphyrinogen I to uroporphyrin I.

Pleiotropic effect of the gene hairless on hepatotoxicity of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin in mice.

Treatment of mice of the A2G-hr/+ congenic line with 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in the development of hepatic porphyria over a period of 4 weeks. Female mice responded to a lesser extent than did males. The degree of porphyria in haired heterozygotes (hr/+) was less than in the corresponding hairless homozygotes (hr/hr) and the haired mice had lower resting metabolic rates than hairless mice. Adaptation of mice of either genotype to a 32-33 degrees C environment resulted in a decrease in resting metabolic rate and a reduction in hepatic porphyrin levels. Histologically-demonstrated necrotic changes in livers were accompanied by increased activity of alanine aminotransferase and sorbitol dehydrogenase in the plasma; however, there was no clear temporal trend in plasma enzyme levels. Elevated environmental temperature reduced the plasma alanine aminotransferase activity. The study provided evidence for a pleiotropic effect of variation at the hr locus being expressed in TCDD hepatotoxicity. Suggestions for mechanisms whereby the effect can be mediated through alterations in resting metabolic rate are made.

Response of murine epidermal keratinocyte cultures to 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD): Comparison of haired and hairless genotypes

Based on the observation that congenic haired and hairless mice differ in the hyperkeratinizing/hyperproliferative epidermal response following topical exposure to 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) in vivo, it has been proposed that this response in mice segregates with the Ah locus (which controls for the Ah receptors) and the hr locus (for hairlessness) ( Knutson and Poland, 1982). In the present studies this hypothesis was tested by comparing the response of epidermal keratinocytes derived from genotypically segregated newborn haired and hairless HRS J mice to TCDD exposure in in vitro cultures. The parameters monitored were stimulation of cell proliferation (as measured by protein content and rate of tritiated thymidine incorporation in cultures), epidermal transglutaminase activity, cornified cell envelope formation, and keratin staining with Rhodanile blue. Results suggested that the sensitivity of HRS J haired and hairless mouse epidermal keratinocyte cultures to TCDD exposure in vitro was very similar. In both cell cultures all parameters monitored were stimulated by TCDD exposure in a similar dose-dependent manner. This suggests that physiologic factors beyond the epidermal cells may be involved in expression of the different responses seen in the skin of mice to TCDD in vivo.

Strain differences in the induction of mono-oxygenase activity in mouse skin by topical clobetasol propionate: Evidence of a role for the hr locus

The effect of the topical application of clobetasol propionate on cutaneous ethoxycoumarin O'dealkylation (EOD) has been studied in various strains of mice. Clobetasol propionate markedly increased cutaneous EOD activity in adult hairless mice only. Similar treatment of adult haired C57BL/6J mice, or adult haired DBA/2J mice had no significant effect on cutaneous EOD activity. In contrast 3 methylcholanthrene induced cutaneous EOD activity in both hairless and C57 strains to a far greater extent than in the DBA strain. EOD activity in hairless mice non-responsive to polycyclic hydrocarbons, derived by selective breeding of hairless and DBA strains was induced by clobetasol propionate to a similar extent to that observed in responsive hairless strains. Hepatic EOD activity was not induced by clobetasol propionate in any of the strains tested. Strain differences in the induction of EOD by clobetasol propionate were not related to differences in either the concentration of cytosolic glucocorticoid receptor in the skin, the dissociation constant of the cytosolic receptor, or differences in percutaneous absorption. Polycyclic hydrocarbons did not compete with triaminolone acetonide for binding to the cytosolic glucocorticoid receptor. Strain differences in the induction of EOD activity by clobetasol propionate appear therefore not to be related to strain differences in either the Ah receptor or the glucocorticoid receptor, but to be regulated by the hr locus.

Four dominant autosomal mutations affecting skin and hair development in the mouse.

Four new dominant autosomal mutations influencing the development of skin and hair in the mouse were tested for allelism with each other and with hairless, hr. Three of the mutations probably constitute an allelic series and have been given the symbols Frl1, Frlb, and Frlc. The Frl series shows no evidence of linkage with hr. The fourth mutation, Hrn, is a dominant and homozygous viable allele at the hr locus. With the possible exception or Frlb, all mutants were of spontaneous origin. Because of their unique characteristics, these new mutants are of potential value as mouse model systems in studies of skin carcinogenesis and related areas of research.

Response of murine epidermis to 2,3,7,8-tetrachlorodibenzo- p-dioxin: Interaction of the Ah and hr loci

2,3,7,8-Tetrachlorodibenzo- p-dioxin (TCDD) and related halogenated aromatic hydrocarbons produce epidermal hyperplasia, hyperkeratosis and sebaceous gland metaplasia in the skin of mice bearing the recessive mutation ( hr/hr) hairless. This response is mediated through the cytosol receptor protein: the structure-activity relationship for receptor binding corresponds to that for production of the skin lesion, and these histopathological changes segregate with the genetic polymorphism at the Ah locus, the locus determining the cytosol receptor. In HRS/J mice, an inbred strain segregating for the hr locus, both hairless ( hr/hr) and haired ( hr/ +) mice possess the high-affinity cytosol receptor and respond to TCDD with the induction of epidermal aryl hydrocarbon hydroxylase activity, a receptor-mediated biochemical response; however, only hr/hr mice develop the proliferative/metaplastic skin response. We propose a genetic model for the interaction of the Ah and hr loci, to account for the differential response to TCDD observed in the skin of HRS/ J hr/hr and hr/ + mice.

Genetics of formamidase-5 (brain formamidase) in the mouse: localization of the structural gene on chromosome 14.

A single formamidase, which is different from the formamidases found in other tissues occurs in the brains of mice. This enzyme is here called formamidase-5 and the gene symbol is designated For-5. Two alleles are recognized on the basis of their differential heat sensitivity:For-5b is relatively heat stable and is present in strain C57BL/6J, while For-5d is relatively heat sensitive and is present in strain DBA/2J. The heat sensitivity of formamidase-5 in 44 other inbred strains and substrains was tested and found to resemble that of C57BL/6J or DBA/2J. Thirty-six recombinant inbred strains derived from progenitors that differed at For-5 were studies to test for single-gene inheritance and linkage with other loci. Complete concordance was found with the esterase-10 locus (Es-10), indicating close linkage. The 99% upper confidence limit of the distance between For-5 and Es-10 is 3.7 centimorgans (cM). Es-10 is located on chromosome 14 about 19 cM from the centromere. An independent demonstration of linkage of For-5 with Es-10 and another chromosome 14 marker, hairless (hr), is provided by the finding that the HRS/J strain, which has been sibmated for 60 generations with forced heterozygosity at the hr locus, is cosegregating at For-5 and Es-10. A survey of 32 inbred strains and substrains revealed that the For-5d allele is associated with the Es-10b allele, and that the For-5b allele is associated with Es-10a and Es-10c. Formamidase-5 segregates as expected in the F2 generation of crosses between strains bearing For-5b and For-5d alleles. It is possible that this unique formamidase of the brain is involved in the metabolism of a neurotransmitter substance.

THE EXPRESSION AND INTERACTION OF HEREDITARY FACTORS AFFECTING HAIR GROWTH IN MICE: EXTERNAL OBSERVATIONS

Macroscopic observations on the expression of two mutant alleles ("hairless" and "rhino") in the house mouse, and on their interaction with one another and with a third mutation ("Naked") producing hypotrichosis of a different type, have been described. In hairless mice the juvenile pelage falls out and the skin shows little wrinkling; rhino mice lose their hair in a similar way but subsequently develop an intense wrinkling of the skin. Naked mice lose their hair by a breaking-off rather than a falling out, and show a pattern of alternate depilation and regeneration of the hair coat.Hairless/rhino hybrids lose their hair according to the hairless pattern, but later manifest a characteristic wrinkling like, but not as extreme as, that of the rhino mutant, "rhino" is therefore not completely recessive to "hairless."There are thus three basic grades of wrinkling—hr/hr, hr/hrrh, hrrh/hrrh—determined by the factors present at the Hr locus. The presence of the heterozygous Naked factor in any of these types causes an intensification of its degree of wrinkling. This intensification is even more pronounced when the Naked factor is homozygous. Moreover, the "Naked" characteristics are themselves exaggerated in these compounds, the intensification being proportional to the degree of wrinkling.These results will be interpreted in the light of histological findings to be presented in the following paper.