Genetic specificity of nitrogen nutrition in leguminous plants

Summary Mineral nitrogen did not increase grain yield and seed protein levels ofVicia faba L. andLupinus luteus L. in field trials and pot experiments. Fixed N₂ was substituted by mineral nitrogen in these cases because of inhibition of N₂ fixation by mineral nitrogen. Contrary to these results mineral nitrogen increased grain yields and seed protein amounts ofLupinus albus L.,Pisum sativum L., andGlycine max. (L.) Merr. The nitrogen effect was caused at an early stage by saving energy due to inhibition of N₂ fixation (measurement of gas exchange by means of IRGA). In case of the N application after flowering grain, yields and seed protein levels increased because the mineral N was an additional nitrogen source for plants. At this stage the plants had ceased fixing atmospheric nitrogen. The high sink activity of growing fruits induced a lack of assimilates in nodules (determined by means of¹⁴CO₂ application). The N effect was therefore the consequence of the lower assimilate pool for supplying root nodules in these plants in comparison withVicia faba L. andLupinus luteus L. Hence it follows that response to mineral nitrogen can be a criterion for discovering more effective Rhizobium-host combinations.     

Genetic factors in individual radiation sensitivity

Cancer risk and radiation sensitivity are often associated with alterations in DNA repair, cell cycle, or apoptotic pathways. Interindividual variability in mutagen or radiation sensitivity and in cancer susceptibility may also be traced back to polymorphisms of genes affecting e.g. DNA repair capacity. We studied possible associations between 70 polymorphisms of 12 DNA repair genes with basal and initial DNA damage and with repair thereof. We investigated DNA damage induced by ionizing radiation in lymphocytes isolated from 177 young lung cancer patients and 169 cancer-free controls. We also sought replication of our findings in an independent sample of 175 families (in total 798 individuals). DNA damage was assessed by the Olive tail moment (OTM) of the comet assay. DNA repair capacity (DRC) was determined for 10, 30 and, 60 min of repair.Genes involved in the single-strand-repair pathway (SSR; like XRCC1 and MSH2) as well as genes involved in the double-strand-repair pathway (DSR; like RAD50, XRCC4, MRE11 and ATM) were found to be associated with DNA damage. The most significant association was observed for marker rs3213334 (p = 0.005) of XRCC1 with basal DNA damage (B), in both cases and controls. A clear additive effect on the logarithm of OTM was identified for the marker rs1001581 of the same LD-block (p = 0.039): B_CC = −1.06 (95%-CI: −1.16 to −0.96), B_CT = −1.02 (95%-CI: −1.11 to −0.93) and B_TT = −0.85 (95%-CI: −1.01 to −0.68). In both cases and controls, we observed significantly higher DNA basal damage (p = 0.007) for carriers of the genotype AA of marker rs2237060 of RAD50 (involved in DSR). However, this could not be replicated in the sample of families (p = 0.781). An alteration to DRC after 30 min of repair with respect to cases was observed as borderline significant for marker rs611646 of ATM (involved in DSR; p = 0.055), but was the most significant finding in the sample of families (p = 0.009).Our data indicate that gene variation impacts measurably on DNA damage and repair, suggesting at least a partial contribution to radiation sensitivity and lung cancer susceptibility.     

Genetic factors in predisposition to bronchial asthma

The ratio between the normal (+) and null (0) alleles of the genes encoding glutatione S-transferases M1 (GSTM1) and T1 (GSTT1) were studied in normal individuals from northwestern Russia (control group) and in patients with bronchial asthma (BA). The frequency of the GSTM1 0/0 genotype in the population sample was statistically significantly lower (37.8%) than in the BA patients (82.1%; chi 2 = 16.8; P < 0.001; w chi 2 = 15.7; alpha = 0.01). For the GSTT1 gene, similar data were obtained. The frequency of the GSTT1 0/0 genotype in healthy donors was statistically significantly higher (16.3%) than in the BA patients (73.7%; chi 2 = 28.5; P < 0.001; w chi 2 = 23.22; alpha = 0.01). A significant preponderance of the compound homozygotes for the GSTM1 and GSTT1 null alleles among the BA patients was observed. The frequency of the GSTM1 0/0, GSTT1 0/0 individuals among the patients was 57.9%, while it was only 4.7% among the controls (chi 2 = 27.4; P < 0.001).     

Genetic and anthropologic factors in gluten-sensitive enteropathy

Gluten-sensitive enteropathy (GSE), a disease characterized by intestinal villous atrophy and malabsorption, is due to a sensitivity to wheat protein, gliadin, and probably has its basis in an underlying immunologic defect. GSE has a genetic basis in that some 70–80% of north American and northern European patients bear the HLA-B8 histocompatibility type and about 90% bear the HLA-DRw3 histocompatibility type. These histocompatibility types are both increased because they are in linkage disequilibrium in normal populations. This suggests that HLA-B8 and HLA-DRw3 genes are in linkage disequilibrium with a GSE disease gene, accounting for the association of the disease with certain histocompatibility antigens. A gene coding for a lymphoid surface antigen has been identified which is not HLA-linked. This gene is distributed at a low frequency in the general population; it has been proposed that both the HLA and non-HLA genes important to GSE code for different domains of the single surface receptor molecule that somehow predisposes to a heightened immune reaction to gliadin, thus causing the disease. GSE is most prevalent where HLA-B8 occurs at the highest frequency in the general population and is not seen in populations where HLA-B8 is not found. One explanation for this is that the gene complex containing HLA-B8 (and HLA-DRw3) evolved in response to infectious agents: Individuals bearing this complex were capable of more vigorous antibody response. However, such individuals were also more likely to be hypersensitive to wheat protein; as wheat became domesticated these individuals may have been at a disadvantage. It is only in regions such as northern Europe where wheat domestication occurred relatively late that one finds both a high frequency of HLA-B8 and a high incidence of GSE.     

Genetic and environmental factors in human osteoporosis

Osteoporosis is a common disorder, with prolongation of the average life span it has become a major public health problem. On the formation of osteoporosis genetic factors and environmental influences could play a role then it is considered as multi-factorial. Because a variety of functions to affect susceptibility to the formation of osteoporosis VDR-F, VDR-B, COL1A1, ESR1X, ESR1P and CTR are thought to be candidate genes. In this study, the aim is to investigate the relationship between these genes polymorphism and bone mineral density (BMD) values of lumbar vertebra and femoral neck in 188 Turkish people. Lumbar spine and femoral neck BMD of the individuals included in the study were measured by the dual X-ray absorptiometry method. The genotyped polymorphisms by simultaneous amplification of five regions of the genome, containing six SNPs of interest and detecting the amplified product, using the kit MetaBone Clinical Arrays^?. Statistical analyses indicated that; VDR-B gene polymorphisms major (P?=?0.013), VDR-F polymorphisms have minor (P?=?0.082) effect on femur BMD. None of the other genes has any significant effect on spinal BMD. Patient age, body mass index and diet has significant effect on femoral and spinal BMD. Osteoporosis is a multi-factorial disease and many genetic and non-genetic risk factors contribute to the development of osteoporosis. Early detection of a genetic predisposition to osteoporosis should allow delay and/or limit unfavorable changes in the bone tissue.     

Genetic risk factors for melanoma

The genetic basis of melanoma is complex and has both inherited and acquired components. Different genomic approaches have been used to identify a number of inherited risk factors, which can be stratified by penetrance and prevalence. Rare high-penetrance factors are expressed in familial clustering of melanoma and include mutations in CDKN2A (encoding p16^INK4a and p14^ARF) and CDK4. These genes are involved in cell-cycle arrest and melanocyte senescence and are nearly invariably targeted by somatic mutations during melanoma progression. Low-penetrance factors are common in the general population and include single-nucleotide polymorphisms in or near MC1R, ASIP, TYR and TYRP1. These genes are major determinants of hair and skin pigmentation, but their role in melanoma development remains unclear. This review describes the efforts that have led to the current understanding of melanoma susceptibility as the result of complex gene–gene and gene–environment interactions. Despite the significant advances, the majority of familial cases remain unaccounted for.     

影响猪肉嫩度的遗传因素

嫩度是猪肉品质的一个重要方面。影响猪肉嫩度的因素很多,遗传因素是改善猪肉嫩度的关键。本对肌纤维性状、钙蛋白酶蛋白水解系统和肌内脂肪的有关基因进行了论述,包括MyoD基因家族、钙调蛋白激酶(CaMK)基因、钙激中性蛋白酶(CAPN)基因、钙蛋白酶抑制蛋白(CAST)基因、心脏脂肪酸结合蛋白(H-FABP)基因、脂肪组织脂肪酸结合蛋白(F一FABP)基因、过氧化氢酶体激活增殖受体（PPARγ)基因以及与肌内脂肪有关的QTL。其中有些已被认为是肉嫩度的候选基因。对改善猪肉嫩度所面临的问题及研究前景进行了讨论。     

Genetic factors underlying prostate cancer

Prostate cancer is one of the leading causes of cancer-related death in the USA. In the past decade, tremendous progress has been made in the identification and understanding of the genetic factors related to prostate cancer development. Unlike many other types of cancers, only a small fraction of prostate cancer cases are aggressive and life-threatening. The factors related to prostate cancer development and progression appear complex and diverse. This review summarises some of the important findings in the areas of genome and gene expression abnormalities in prostate cancer, and aims to provide a comprehensive view of new developments in these areas.     

Genetic factors and malaria in the Temuan.

The jungle habitat of the Temuan aborigines harbors a variety of infectious diseases, the most notable being malaria. Our study of 15 genetic systems in the Temuan revealed substantial polymorphism and within-population genetic diversity. The polymorphisms for Hb beta, G6PD, and El are of interest in regard to genetic adaptation to malaria. Among the polymorphisms investigated we conclude that G6PD deficiency and elliptocytosis are likely to have malaria-resistant effects as evidenced by their low association with malarial parasitemia or their higher frequency in adults than in children. These findings suggest that the malarial habitat of the Temuans is livable in the long range sense for them because of the cluster of malaria-resistant alleles in their gene pool (G6PD)-, El, and possibly, but not tested here because of its low frequency, Hb beta E). The same condition probably holds for the Semai, the nearest aborigine neighbors of the Temuan (although the Semai have not been tested for malarial parasitemia and for these polymorphisms simultaneously), since the Semai have substantial Hb betaE, G6PD-, and El. The Temuan have a cultural identity system of rituals, beliefs, and certain aspects of language which effectively isolates them genetically from Malays and other nonaborigines. This system hinders the dilution of the malaria-resistant alleles of the Temuan gene pool with the malaria-susceptible alleles of the nonaborigine gene pools.