Island Formation History Determines Microbial Species-Area Relationships.

The species-area relationship (SAR) and its mechanisms regarding microbes are not as clear as those of plants and animals; this may result from the impact of sampling effects and the confusion between SAR and distance attenuation. We hypothesize that we can find more accurate microbial SAR curve, after removing these two factors. In this study, 27 leaves of three horticultural plants were selected as island models, and microbial biodiversity assessment was done with HTS (high-throughput sequencing). The separate and small systems using leaves as islands allow us to conduct a comprehensive survey of the microbial biodiversity of the leaves, without disturbance from sampling effects and distance attenuation effects. Interestingly, we did not find microbial SAR in those 27 leaves (also not found in evergreen trees Magnolia grandiflora and Eriobotrya japonica), but we did find significant microbial SAR in deciduous tree Ficus altissima. No significant differences were found between the different trees at the alpha diversity level of microbial biodiversity, but quite different on beta diversity. The results of beta diversity partition showed that F. altissima had the highest similarity of the microbial community among the leaves compared to those of M. grandiflora and E. japonica. Since leaf genesis in deciduous plants is more simultaneous than in evergreen plants; the result suggested that inconsistent historical background of leaf islands may mask microbial SAR. Thus, intensive sampling and consistent historical background are important for understanding microbial SAR.

Sampling methods affect Nematode-Trapping Fungi biodiversity patterns across an elevational gradient.

BACKGROUND: Understanding the patterns of species richness across elevational gradients is a key concept for contemporary research in ecology and evolution, and critical to understanding large-scale trends in biodiversity, global change and conservation. However, patterns of elevational species richness between taxonomic groups, regions and latitudes are inconsistent, so that various, sometimes conflicting hypotheses exist. Several scholars have pointed out that research on elevational distribution patterns is often biased by the sampling design employed. To test this hypothesis, we analyzed species richness of Nematode-Trapping Fungi (NTF) across an elevation gradient at two mountainous sites in western Yunnan Province, P.R. China. We tested for potential differences in the results when using different sampling designs. RESULTS: A total of 3 genera, 17 species, 222 strains of NTF were isolated and identified from Gaoligongshan and Cangshan. Species accumulation curves for both sites and sampling modes had acceptable leveling, demonstrating sufficient sampling effort. At Gaoligongshan, the elevation distribution patterns of NTF were different under two sampling patterns. When reducing the analyzed altitude range in Gaoligongshan, the elevation distribution pattern of the NTF changed. A similar elevation distribution pattern was observed in Cangshan when testing the same altitude range. In general, when treating the same dataset using different sampling designs, the resulting distribution patterns of species richness and occurrence frequencies were clearly different. Moreover, after removal of the samples located within lower-altitude zones affected by anthropogenic interferences, the distribution pattern of NTF in the two sites tended to become uniform. CONCLUSION: The sampling design, and in particular the elevation interval between plots, has a significant effect on the assessment of species distribution in mountainous regions. Other factors such as human activities and the multi-dimensionality of biodiversity also contribute to result biases. It is recommended that sampling design is given careful consideration in future studies on the elevational gradients of species richness, using stratified approaches according to the most relevant factors.

Polymorphism in DNMT1 may modify the susceptibility to oligospermia.

As an important methyltransferase, DNMT1 plays a key role in DNA methylation that is essential for normal spermatogenesis, which suggests that it may be involved in male infertility with spermatogenesis impairment. To explore the relationship between DNMT1 and spermatogenesis impairment, polymorphic distributions of single-nucleotide polymorphisms (SNP) rs16999593, rs2228612 and rs2228611 in DNMT1 were investigated in 342 infertile patients with idiopathic azoospermia or oligospermia and 232 fertile controls in a Chinese population. As a result, no significant differences in allele and genotype frequencies of the three SNP between total patients and controls were observed. However, after stratifying the patients, significant differences in allele and genotype frequencies were detected between oligospermia subgroup and control group. The frequencies of rs16999593 allele A (83.6% versus 77.6%, P=0.033) and genotype AA (69.2% versus 59.0%, P=0.037) and SNP rs2228611 genotype AA (18.4% versus 9.9%, P=0.016) in patients with oligospermia were significantly higher than those in control group. These findings suggest that the polymorphism in DNMT1 might be associated with oligospermia and could modify the susceptibility of oligospermia.

SNPs in KIT and KITLG genes may be associated with oligospermia in Chinese population.

KIT/KITLG signaling system is crucial for spermatogenesis, which suggests that KIT and KITLG genes may be involved in spermatogenesis impairment and male infertility. To explore the possible association of KIT and KITLG genes with male infertility having spermatogenesis impairment, polymorphism distributions of SNP rs3819392 in KIT gene as well as rs995030 and rs4474514 in KITLG gene were investigated in 372 patients with idiopathic azoospermia or oligospermia and 205 fertile controls. As a result, the significant differences in polymorphism distributions of SNP rs3819392 in KIT gene and rs4474514 in KITLG gene were observed between the patients with oligospermia and controls. The frequencies of allele G (94.2% versus 90.0% p = 0.022) and genotype GG (89.2% versus 82.0% p = 0.042) in patients with oligospermia were significantly higher than those in controls at rs3819392 locus in KIT gene. In addition, the genotype CC of rs4474514 in KITLG (8.2% versus 3.4%, p = 0.034) also significantly increased in oligospermic patients in comparison to controls. These findings indicated that SNP rs3819392 in KIT gene and rs4474514 in KITLG gene may be associated with oligospermia, suggesting that polymorphism of KIT and KITLG genes may play a role in oligospermia.

Genetic variants of eNOS gene may modify the susceptibility to idiopathic male infertility.

In testis, eNOS is responsible for synthesis of nitric oxide (NO) which is an essential gas message regulator in spermatogenesis, suggesting that eNOS gene plays a role in normal spermatogenesis and the genetic variants of eNOS gene may be potential genetic risk factors of spermatogenesis impairment. In this study, the polymorphic distributions of three common polymorphism loci including T-786C, 4A4B and G894T in eNOS gene were investigated in 355 Chinese infertile patients with azoospermia or oligozoospermia and 246 healthy fertile men and a meta-analysis was carried in order to explore the possible relationship between the three loci of eNOS gene and male infertility with spermatogenesis impairment. As a result, allele -786C of T-786C (11.4% versus 6.5%, p = 0.004) and 4A of 4A4B (11.0% versus 6.3%, p = 0.005) as well as genotype TC of T-786C (22.8% versus 13.0%, p = 0.002) and AB of 4A4B (18% versus 11%, p = 0.015) were significantly associated with idiopathic male infertility. The haplotypes T-4A-G (7.4% versus 4.1%, p = 0.015) and C-4B-G (7.6% versus 4.4%, p = 0.028) could increase the susceptibility to male infertility, whereas haplotype T-4B-G (67.0% versus 75.2%, p = 0.002) might be a protective factor for male infertility. The results of meta-analysis revealed that the polymorphism of T-786C was associated with male infertility. These findings suggested that the variants of eNOS gene may modify the susceptibility to male infertility with impaired spermatogenesis.

Association of GSTM1 and GSTT1 genes with the susceptibility to male infertility: result from a meta-analysis.

The deletion polymorphisms of the glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1) genes were considered as candidates for genetic susceptibility factors of male infertility. Previous studies concerning the relationship between the null genotype of the two genes and male infertility have been reported in recent years. However, the results remain elusive. A meta-analysis was performed to estimate the relationship between the deletion polymorphism of the GSTM1 or GSTT1 gene, and male infertility in this study. Sixteen studies concerning the GSTM1 gene, including 2174 cases and 1861 controls, and 13 case-control studies on the GSTT1 gene with a total number of 1992 cases and 1617 controls were processed. The results showed that the null genotype of the GSTM1 gene was associated with male infertility in the overall populations (P=0.003, OR=1.40, 95%CI=1.12-1.75), especially in Caucasian (P=0.012, OR=1.50, 95%CI=1.09-2.07) as well as Chinese (P=0.001, OR=1.55, 95%CI=1.19-2.03). The null genotype of the GSTT1 gene was strongly related to male infertility only in Chinese (P=0.000, OR=1.70, 95%CI=1.34-2.14). These results indicated that the null genotype of the GSTM1 gene might contribute to the susceptibility of male infertility, whereas the null genotype of the GSTT1 gene may be a genetic susceptibility factor of male infertility for the Chinese.

Null genotype of GSTM1 and GSTT1 may contribute to susceptibility to male infertility with impaired spermatogenesis in Chinese population.

Glutathione-S-transferases (GSTs) play a protective role during spermatogenesis and GST genes may be involved in impaired spermatogenesis. A case-control study was performed to explore the association of genes GSTM1 and GSTT1, two members of GST gene family, with spermatogenesis impairment. The deletion polymorphism distribution of genes GSTM1 and GSTT1 was investigated in 353 patients with azoospermia or oligospermia and 201 fertile controls in Chinese population using multiplex PCR. As a result, the frequencies of null genotype of genes GSTM1 (67.4% versus 57.7%, p = 0.022, OR = 1.516, 95% CI = 1.001-2.168) and GSTT1 (61.8% versus 46.8%, p = 0.001, OR = 1.838, 95% CI = 1.295-2.610) in patients were significantly higher than those in controls. After stratifying patients, the frequencies of null genotype of gene GSTM1 in oligospermia (68.3% versus 57.7%, p = 0.027, OR = 1.580, 95% CI = 1.051-2.375) and GSTT1 in azoospermia (66.9% versus 46.8%, p < 0.001, OR = 2.299, 95% CI = 1.484-3.562) as well as oligospermia (57.9% versus 46.8%, p = 0.025, OR = 1.567, 95% CI = 1.057-2.322) were still significantly higher compared with controls. The results suggested that null genotypes of GSTM1 and GSTT1 are associated with spermatogenesis impairment and may contribute to susceptibility to spermatogenesis impairment and male infertility in Chinese population.