Fun30 chromatin remodeler helps in dealing with torsional stress and camptothecin-induced DNA damage.

Fun30 is an ATP-dependent chromatin remodeler in budding yeast that is involved in cellular processes important for maintaining genomic stability such as gene silencing and DNA damage repair. Cells lacking Fun30 are moderately sensitive to the topoisomerase inhibitor camptothecin and exhibit a delay in cell cycle progression in the presence of camptothecin. Here, we show that Fun30 is required to cope with torsional stress in the absence of Top1.

Electrical detection of blood cells in urine.

Available methods for detecting blood in the urine (hematuria) can be problematic since results can be influenced by many factors in patients and in the lab settings, resulting in false positive or false negative results. This necessitates the development of new, accurate and easy-access methods that save time and effort. This study demonstrates a label-free and accurate method for detecting the presence of red and white blood cells (RBCs and WBCs) in urine by measuring the changes in the dielectric properties of urine upon increasing concentrations of both cell types.

SMARCAD1 in Breast Cancer Progression.

Background/aims: Breast cancer is the most common cancer in women worldwide, and within this cancer type, triple-negative breast cancers have the worst prognosis. The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-cancer targeted therapies, which could lead to a better management of these patients. In this context, we have recently demonstrated that SMARCAD1, a DEAD/H box-containing helicase, is involved in breast cancer cell migration, invasion, and metastasis.

Repair of Oxidative DNA Damage in Saccharomyces cerevisiae.

Malfunction of enzymes that detoxify reactive oxygen species leads to oxidative attack on biomolecules including DNA and consequently activates various DNA repair pathways. The nature of DNA damage and the cell cycle stage at which DNA damage occurs determine the appropriate repair pathway to rectify the damage. Oxidized DNA bases are primarily repaired by base excision repair and nucleotide incision repair.

Effect of salt on the binding of the linker histone H1 to DNA and nucleosomes.

The linker histones are involved in the salt-dependent folding of the nucleosomes into higher-order chromatin structures. To better understand the mechanism of action of these histones in chromatin, we studied the interactions of the linker histone H1 with DNA at various histone/DNA ratios and at different ionic strengths. In direct competition experiments, we have confirmed the binding of H1 to superhelical DNA in preference to linear or nicked circular DNA forms.

Selective recognition of acetylated histones by bromodomains in transcriptional co-activators.

Bromodomains are present in many chromatin-associated proteins such as the SWI/SNF and RSC chromatin remodelling and the SAGA HAT (histone acetyltransferase) complexes, and can bind to acetylated lysine residues in the N-terminal tails of the histones. Lysine acetylation is a histone modification that forms a stable epigenetic mark on chromatin for bromodomain-containing proteins to dock and in turn regulate gene expression. In order to better understand how bromodomains read the 'histone code' and interact with acetylated histones, we have tested the interactions of several bromodomains within transcriptional co-activators with differentially acetylated histone tail peptides and HAT-acetylated histones.