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Male Feminization of the Common Pillbug Armadillidium vulgare by Wolbachia bacteria

Ramanan et al. | Jun 30, 2024

Male Feminization of the Common Pillbug <i>Armadillidium vulgare</i> by <i>Wolbachia</i> bacteria
Image credit: Ramanan et al. 2024

Wolbachia pipientis (Wolbachia) is a maternally inherited endosymbiotic bacterium that infects over 50% of arthropods, including pillbugs, and acts as a reproductive parasite in the host. In the common terrestrial pillbug Armadillidium vulgare (A. vulgare), Wolbachia alters the sex ratio of offspring through a phenomenon called feminization, where genetic males develop into reproductive females. Previous studies have focused on the presence or absence of Wolbachia as a sex ratio distorter in laboratory cultured and natural populations mainly from sites in Europe and Japan. Our three-year study is the first to evaluate the effects of the Wolbachia sex ratio distorter in cultured A. vulgare offspring in North America. We asked whether Wolbachia bacteria feminize A. vulgare isopod male offspring from infected mothers and if this effect can be detected in F1 offspring by comparing the male/female offspring ratios. If so, the F1 offspring ratio should show a higher number of females than males compared to the offspring of uninfected mothers. Over three years, pillbug offspring were cultured from pregnant A. vulgare females and developed into adults. We determined the Wolbachia status of mothers and counted the ratios of male and female F1 progeny to determine feminization effects. In each year sampled, significantly more female offspring were born to Wolbachia-infected mothers than those from uninfected mothers. These ratio differences suggest that the Wolbachia infection status of mothers directly impacts the A. vulgare population through the production of reproductive feminized males, which in turn provides an advantage for further Wolbachia transmission.

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Development of a Novel Treatment Strategy to Treat Parkinsonian Neurodegeneration by Targeting Both Lewy Body Aggregation and Dopaminergic Neuronal Degradation in a Drosophila melanogaster Model

Sama et al. | Sep 25, 2019

Development of a Novel Treatment Strategy to Treat Parkinsonian Neurodegeneration by Targeting Both Lewy Body Aggregation and Dopaminergic Neuronal Degradation in a <em>Drosophila melanogaster</em> Model

In this article the authors address the complex and life quality-diminishing neurodegenerative disease known as Parkinson's. Although genetic and/or environmental factors contribute to the etiology of the disease, the diagnostic symptoms are the same. By genetically modifying fruit flies to exhibit symptoms of Parkinson's disease, they investigate whether drugs that inhibit mitochondrial calcium uptake or activate the lysosomal degradation of proteins could improve the symptoms of Parkinson's these flies exhibit. The authors report the most promising outcome to be that when both types of drugs were used together. Their data provides encouraging evidence to support further investigation of the utility of such drugs in the treatment of human Parkinson's patients.

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siRNA-dependent KCNMB2 silencing inhibits lung cancer cell proliferation and promotes cell death

Jeong et al. | Nov 01, 2022

siRNA-dependent KCNMB2 silencing inhibits lung cancer cell proliferation and promotes cell death

Here, seeking to better understand the genetic associations underlying non-small cell lung cancer, the authors screened hundreds of genes, identifying that KCNMB2 upregulation was significantly correlated with poor prognoses in lung cancer patients. Based on this, they used small interfering RNA to decrease the expression of KCNMB2 in A549 lung cancer cells, finding decreased cell proliferation and increased lung cancer cell death. They suggest this could lead to a new potential target for lung cancer therapies.

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String analysis of exon 10 of the CFTR gene and the use of Bioinformatics in determination of the most accurate DNA indicator for CF prediction

Carroll et al. | Jul 12, 2020

String analysis of exon 10 of the CFTR gene and the use of Bioinformatics in determination of the most accurate DNA indicator for CF prediction

Cystic fibrosis is a genetic disease caused by mutations in the CFTR gene. In this paper, the authors attempt to identify variations in stretches of up to 8 nucleotides in the protein-coding portions of the CFTR gene that are associated with disease development. This would allow screening of newborns or even fetuses in utero to determine the likelihood they develop cystic fibrosis.

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The effect of Omega-3 on bovine blood cells as a potential remedy for Cerebral Cavernous Malformations

Pulluru et al. | Sep 22, 2023

The effect of Omega-3 on bovine blood cells as a potential remedy for Cerebral Cavernous Malformations
Image credit: Carolien van Oijen

Here, the authors investigated if dietary Omega-3 fatty acids could reduce the potential for cerebral cavernous malformations, which are brain lesions that occur due to a genetic mutation where high membrane permeability occurs between endothelial cell junctions. In a bovine-based study where some cows were fed an Omega-3 diet, the authors found the membranes of bovine blood cells increased in thickness with Omega-3 supplementation. As a result, they suggest that dietary Omega-3 could be considered as a possible preventative measure for cerebral cavernous malformations.

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Can Children Acquire Their Parents’ History of Fracture?

Boulis et al. | Sep 24, 2018

Can Children Acquire Their Parents’ History of Fracture?

While the genetic basis of hip fracture risk has been studied extensively in adults, it is not known whether parental history of bone fractures affects their children's fracture risk. In this article, the authors investigated whether a parental history of bone fractures influences the rate of fractures in their children. They found that adolescent children whose parents had a more extensive history of fractures were more likely to have a history of fractures themselves, suggesting that parents' medical histories may be an important consideration in future pediatric health research.

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Contrasting role of ASCC3 and ALKBH3 in determining genomic alterations in Glioblastoma Multiforme

Sriram et al. | Sep 27, 2022

Contrasting role of <i>ASCC3</i> and <i>ALKBH3</i> in determining genomic alterations in Glioblastoma Multiforme

Glioblastoma Multiforme (GBM) is the most malignant brain tumor with the highest fraction of genome alterations (FGA), manifesting poor disease-free status (DFS) and overall survival (OS). We explored The Cancer Genome Atlas (TCGA) and cBioportal public dataset- Firehose legacy GBM to study DNA repair genes Activating Signal Cointegrator 1 Complex Subunit 3 (ASCC3) and Alpha-Ketoglutarate-Dependent Dioxygenase AlkB Homolog 3 (ALKBH3). To test our hypothesis that these genes have correlations with FGA and can better determine prognosis and survival, we sorted the dataset to arrive at 254 patients. Analyzing using RStudio, both ASCC3 and ALKBH3 demonstrated hypomethylation in 82.3% and 61.8% of patients, respectively. Interestingly, low mRNA expression was observed in both these genes. We further conducted correlation tests between both methylation and mRNA expression of these genes with FGA. ASCC3 was found to be negatively correlated, while ALKBH3 was found to be positively correlated, potentially indicating contrasting dysregulation of these two genes. Prognostic analysis showed the following: ASCC3 hypomethylation is significant with DFS and high ASCC3 mRNA expression to be significant with OS, demonstrating ASCC3’s potential as disease prediction marker.

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