Genetic and ultrastructural analysis reveals the key players and initial steps of bacterial magnetosome membrane biogenesis

Magnetosomes of magnetotactic bacteria contain well-ordered nanocrystals for magnetic navigation and have recently emerged as the most sophisticated model system to study the formation of membrane bounded organelles in prokaryotes. Magnetosome biosynthesis is thought to begin with the formation of a dedicated compartment, the magnetosome membrane (MM), in which the biosynthesis of a magnetic mineral is strictly controlled. While the biomineralization of magnetosomes and their subsequent assembly into linear chains recently have become increasingly well studied, the molecular mechanisms and early stages involved in MM formation remained poorly understood. In the Alphaproteobacterium Magnetospirillum gryphiswaldense, approximately 30 genes were found to control magnetosome biosynthesis. By cryo-electron tomography of several key mutant strains we identified the gene complement controlling MM formation in this model organism. Whereas the putative magnetosomal iron transporter MamB was most crucial for the process and caused the most severe MM phenotype upon elimination, MamM, MamQ and MamL were also required for the formation of wild-type-like MMs. A subset of seven genes (mamLQBIEMO) combined within a synthetic operon was sufficient to restore the formation of intracellular membranes in the absence of other genes from the key mamAB operon. Tracking of de novo magnetosome membrane formation by genetic induction revealed that magnetosomes originate from unspecific cytoplasmic membrane locations before alignment into coherent chains. Our results indicate that no single factor alone is essential for MM formation, which instead is orchestrated by the cumulative action of several magnetosome proteins

Kontrolle von Rhizoctonia solani in Kartoffeln mit einer neu entwickelten Reihenapplikationstechnik von suppressiven Komposten

The soil borne pathogen Rhizoctonia solani is of increasing importance since organic seed potatoes are compulsory in organic potato production. No convincing measure to control the disease is available for organic production. The effect of a suppressive compost mixture of organic household and yard waste to control R. solani in potatoes was tested in an organic field trial at the University Kassel in 2006. The compost was directly applied at the seed tuber area. Seed tubers (variety Nicola) naturally infested with black scurf were planted in three infection classes (no, middle and high infection). Compost amendment had a strong impact on symptoms of R. solani on tubers. The reduction of both the infestation of harvested potatoes with black scurf and the rate of tubers with deformations and dry core was significant at final harvest. Although the rate of initial infection of the seed tubers had an impact on tuber health and quality the disease was reduced up to 50% in all infection classes. These promising results en-courage increasing the research on a development of a strip application technique of composts to control the disease

The Complex Roles of Adipokines in Polycystic Ovary Syndrome and Endometriosis

Polycystic ovary syndrome (PCOS) and endometriosis are frequent diseases of the female reproductive tract causing high morbidity as they can significantly affect fertility and quality of life. Adipokines are pleiotropic signaling molecules secreted by white or brown adipose tissues with a central role in energy metabolism. More recently, their involvement in PCOS and endometriosis has been demonstrated. In this review article, we provide an update on the role of adipokines in both diseases and summarize previous findings. We also address the results of multi-omics approaches in adipokine research to examine the role of single nucleotide polymorphisms (SNPs) in genes coding for adipokines and their receptors, the secretome of adipocytes and to identify epigenetic alterations of adipokine genes that might be conferred from mother to child. Finally, we address novel data on the role of brown adipose tissue (BAT), which seems to have notable effects on PCOS. For this review, original research articles on adipokine actions in PCOS and endometriosis are considered, which are listed in the PubMed database

Estrogen receptor β is associated with expression of cancer associated genes and survival in ovarian cancer

BackgroundIn ovarian cancer, the role of estrogen receptors (ERs), particularly of ER, being suggested as tumor suppressor in breast and prostate cancer, remains unclear. We examined the expression of nuclear and cytoplasmic ER in ovarian cancer and correlated it with expression of ovarian cancer markers CA125, CEA and CA72-4, steroid hormone receptors ER and PR, cancer-associated genes EGFR, p53, HER2 and proliferation marker Ki-67. Additionally we examined to what extent expression of ER and the other proteins affects survival of ovarian cancer patients.MethodsWe established a tissue microarray from 171 ovarian cancer patients and performed immunohistochemical analyses of the mentioned proteins.ResultsNuclear ER was detected in 47.31% of the ovarian cancer tissues and cytoplasmic expression of this receptor was observed in 23.08%. Nuclear expression of ER was significantly decreased in the G3 subgroup compared to better differentiated cancers (p<0.01) and correlated with ovarian cancer markers CEA (95% CI 0.1598-0.4465; p<0.0001) and CA72-4 (95% CI 0.05953-0.3616; p<0.01). Cytoplasmic ER expression correlated with EGFR levels (95% CI 0.1059-0.4049; p<0.001). ER expression was associated with expression of CA125 and PR. Overall survival of patients with tumors expressing cytoplasmic ER was significant longer compared to those with ER-negative ovarian cancer (chi-square statistic of the log-rank, p<0.05). Progression-free survival was dependent on expression of PR (chi-square statistic of the log-rank, p<0.05) and Ki-67 (p=0.05).ConclusionsOur data suggest an important, but distinct role of nuclear and cytoplasmic ER expression in ovarian cancer and encourage further studies on its role in this cancer entity

Role of Estrogen Receptor β, G-Protein Coupled Estrogen Receptor and Estrogen-Related Receptors in Endometrial and Ovarian Cancer

Ovarian and endometrial cancers are affected by estrogens and their receptors. It has been long known that in different types of cancers, estrogens activate tumor cell proliferation via estrogen receptor α (ERα). In contrast, the role of ERs discovered later, including ERβ and G-protein-coupled ER (GPER1), in cancer is less well understood, but the current state of knowledge indicates them to have a considerable impact on both cancer development and progression. Moreover, estrogen related receptors (ERRs) have been reported to affect pathobiology of many tumor types. This article provides a summary and update of the current findings on the role of ERβ, GPER1, and ERRs in ovarian and endometrial cancer. For this purpose, original research articles on the role of ERβ, GPER1, and ERRs in ovarian and endometrial cancers listed in the PubMed database have been reviewed

Icb-1 gene polymorphism rs1467465 is associated with susceptibility to ovarian cancer

In this study, we tested the hypothesis that single nucleotide polymorphisms (SNPs) of differentiation-associated human gene icb-1 (C1orf38) may be associated with ovarian cancer susceptibility. For this purpose, we compared the genotype and allele frequencies of the SNPs rs1467465 and rs12048235 in a group of 184 ovarian cancer patients with a control group of 184 age- and gender-matched women without any malignancy. Genotype-phenotype association revealed that A allele of SNP rs1467465 was more frequent in ovarian cancer patients than in the control group (0.40 vs. 0.33, OR 1.37, 95% CI 1.013-1.853, p = 0.04). After analysis of allele positivity we observed that A-positive genotypes were more frequent in the ovarian cancer group (0.65 vs. 0.53, OR 1.63, 95% CI 1.072-2.483, p = 0.02). Furthermore, the heterozygous genotype of rs1467465 was found to be more frequent in the patients group (0.50 vs. 0.41, OR 1.63, 95% CI 1.045-2.045, p = 0.03). No significant results were obtained with regard to SNP rs1204823. Our data suggest, that SNP rs1467465 of human gene icb-1 might affect susceptibility to ovarian cancer

Icb-1 gene polymorphism rs1467465 is associated with susceptibility to ovarian cancer

In this study, we tested the hypothesis that single nucleotide polymorphisms (SNPs) of differentiation-associated human gene icb-1 (C1orf38) may be associated with ovarian cancer susceptibility. For this purpose, we compared the genotype and allele frequencies of the SNPs rs1467465 and rs12048235 in a group of 184 ovarian cancer patients with a control group of 184 age- and gender-matched women without any malignancy. Genotype-phenotype association revealed that A allele of SNP rs1467465 was more frequent in ovarian cancer patients than in the control group (0.40 vs. 0.33, OR 1.37, 95% CI 1.013-1.853, p = 0.04). After analysis of allele positivity we observed that A-positive genotypes were more frequent in the ovarian cancer group (0.65 vs. 0.53, OR 1.63, 95% CI 1.072-2.483, p = 0.02). Furthermore, the heterozygous genotype of rs1467465 was found to be more frequent in the patients group (0.50 vs. 0.41, OR 1.63, 95% CI 1.045-2.045, p = 0.03). No significant results were obtained with regard to SNP rs1204823. Our data suggest, that SNP rs1467465 of human gene icb-1 might affect susceptibility to ovarian cancer

Agonists and knockdown of estrogen receptor β differentially affect invasion of triple-negative breast cancer cells in vitro

Background: Estrogen receptor beta (ER beta) is expressed in the majority of invasive breast cancer cases, irrespective of their subtype, including triple-negative breast cancer (TNBC). Thus, ER beta might be a potential target for therapy of this challenging cancer type. In this in vitro study, we examined the role of ER beta in invasion of two triple-negative breast cancer cell lines. Methods: MDA-MB-231 and HS578T breast cancer cells were treated with the specific ER beta agonists ERB-041, WAY200070, Liquiritigenin and 3 beta-Adiol. Knockdown of ER beta expression was performed by means of siRNA transfection. Effects on cellular invasion were assessed in vitro by means of a modified Boyden chamber assay. Transcriptome analyses were performed using Affymetrix Human Gene 1.0 ST microarrays. Pathway and gene network analyses were performed by means of Genomatix and Ingenuity Pathway Analysis software. Results: Invasiveness of MBA-MB-231 and HS578T breast cancer cells decreased after treatment with ER beta agonists ERB-041 and WAY200070. Agonists Liquiritigenin and 3 beta-Adiol only reduced invasion of MDA-MB-231 cells. Knockdown of ER beta expression increased invasiveness of MDA-MB-231 cells about 3-fold. Transcriptome and pathway analyses revealed that ER beta knockdown led to activation of TGF beta signalling and induced expression of a network of genes with functions in extracellular matrix, tumor cell invasion and vitamin D3 metabolism. Conclusions: Our data suggest that ER beta suppresses invasiveness of triple-negative breast cancer cells in vitro. Whether ER beta agonists might be useful drugs in the treatment of triple-negative breast cancer, has to be evaluated in further animal and clinical studies