Search

Corvids, including the European hooded crow (Corvus cornix), account for a significant proportion of the thousands of wild birds admitted to wildlife rehabilitation centers worldwide. Limiting stress related to captivity and providing sufficient cognitive stimulation for these highly intelligent birds remains a challenge. In this study, we attempted to use music as environmental enrichment for crows rehabilitated in the Warsaw Zoo Rehabilitation Center (Ptasi Azyl) during the summer of 2019. Our results suggest that exposure to music had a calming effect on the birds, encouraging normal activities and reducing the incidence of stress-related behaviors. [ABSTRACT FROM AUTHOR]

The mitochondrial genome of the pathogenic yeast Candida albicans displays a typical organization of several (eight) primary transcription units separated by noncoding regions. Presence of genes encoding Complex I subunits and the stability of its mtDNA sequence make it an attractive model to study organellar genome expression using transcriptomic approaches. The main activity responsible for RNA degradation in mitochondria is a two-component complex (mtEXO) consisting of a 3ʹ-5ʹ exoribonuclease, in yeasts encoded by the DSS1 gene, and a conserved Suv3p helicase. In C. albicans, deletion of either DSS1 or SUV3 gene results in multiple defects in mitochondrial genome expression leading to the loss of respiratory competence. Transcriptomic analysis reveals pervasive transcription in mutants lacking the mtEXO activity, with evidence of the entire genome being transcribed, whereas in wild-type strains no RNAs corresponding to a significant fraction of the noncoding genome can be detected. Antisense ('mirror') transcripts, absent from normal mitochondria are also prominent in the mutants. The expression of multiple mature transcripts, particularly those translated from bicistronic mRNAs, as well as those that contain introns is affected in the mutants, resulting in a decreased level of proteins and reduced respiratory complex activity. The phenotype is most severe in the case of Complex IV, where a decrease of mature COX1 mRNA level to ~5% results in a complete loss of activity. These results show that RNA degradation by mtEXO is essential for shaping the mitochondrial transcriptome and is required to maintain the functional demarcation between transcription units and non-coding genome segments. [ABSTRACT FROM AUTHOR]

Abstract Vulvar squamous cell carcinoma (VSCC) is a rare female genital neoplasm. Although numerous molecular changes have been reported in VSCC, biomarkers of clinical relevance are still lacking. On the other hand, there is emerging evidence on the use of mtDNA as a diagnostic tool in oncology. In order to investigate mtDNA status in VSCC patients, haplogroup distribution analysis and D-loop sequencing were performed. The results were compared with available data for the general Polish population, cancer free-centenarians as well as patients with endometrial and head and neck cancer. The obtained data were also compared with the current status of mitochondrial databases. Significant differences in haplogroup distribution between VSCC cohort, general Polish population and cancer-free centenarians cohort were found. Moreover, a correlation between the VSCC patients haplogroup and HPV status was observed. Finally, a specific pattern of mtDNA polymorphisms was found in VSCC. Our results suggest that the mitochondrial genetic background may influence the risk of VSCC occurrence as well as susceptibility to HPV infection.

Pentatricopeptide repeat (PPR) proteins bind RNA and are present in mitochondria and chloroplasts of Eukaryota. In fungi, they are responsible for controlling mitochondrial genome expression, mainly on the posttranscriptional level. Candida albicans is a human opportunistic pathogen with a facultative anaerobic metabolism which, unlike the model yeast Saccharomyces cerevisiae , possesses mitochondrially encoded respiratory Complex I (CI) subunits and does not tolerate loss of mtDNA. We characterized the function of 4 PPR proteins of C. albicans that lack orthologs in S. cerevisiae and found that they are required for the expression of mitochondrially encoded CI subunits. We demonstrated that these proteins localize to mitochondria and are essential to maintain the respiratory capacity of cells. Deletion of genes encoding these PPR proteins results in changes in steady-state levels of mitochondrial RNAs and proteins. We demonstrated that C. albicans cells lacking CaPpr4, CaPpr11, and CaPpr13 proteins show no CI assembly, whereas the lack of CaPpr7p results in a decreased CI activity. CaPpr13p is required to maintain the bicistronic NAD4L–NAD5 mRNA, whereas the other 3 PPR proteins are likely involved in translation-related assembly of mitochondrially encoded CI subunits. In addition, we show that CaAep3p, which is an ortholog of ScAep3p, performs the evolutionary conserved function of controlling expression of the ATP8–ATP6 mRNA. We also show that C. albicans cells lacking PPR proteins express a higher level of the inducible alternative oxidase (AOX2) which likely rescues respiratory defects and compensates for oxidative stress. [ABSTRACT FROM AUTHOR]

Cancers account for 85% of renal tumors. In Poland renal cancer is diagnosed in almost four thousands patients every year and two thousands of them dies. The most common subtype of renal cancer is clear cell renal cell carcinoma (ccRCC), which accounts for 80-90% of all renal cancer cases. ccRCC is resistant to chemo- and radiotherapy. More and more data suggest that tumor growth is a result of proliferation and differentiation of a small population of cells called cancer stem cells (CSC). CSCs are responsible for tumor progression and for the resistance to chemo- and radiotherapy. This publication covers the role the CSCs and their origin in renal cell carcinoma, with particular emphasis on clear cell subtype.

Current state-of-the-art anti-angiogenic therapies target the VEGF pathway, which is the main essential signaling pathway for angiogenesis, including pathological angiogenesis in cancer and eye disease. Ranibizumab (Lucentis) and VEGF-Trap (aflibercept) represent two different approaches to inhibiting angiogenesis by targeting VEGF family signaling. The former is a relatively short monoclonal antibody fragment, which binds VEGF-A on the basis of antigen recognition by the variable region of an antibody, while aflibercept is not an monoclonal antibody, but a decoy receptor, binding VEGF-A on the basis of the molecular interaction between the ligand (VEGF) and its cognate cellular receptor (VEGFR-1 and VEGFR-2). VEGF-Trap has therefore a broader specificity, recognizing and binding VEGF-B and PIGF in addition to VEGF-A, following the specificity of VEGFR-1 and VEGFR-2. This broader specificity is considered as beneficial in cancer treatment and could be also beneficial in treatment of nAMD, this claim should, however, be backed by clinical studies. The presence of an Fc fragment in VEGF-Trap is also an important difference; even though this fragment does not participate in the recognition of the target molecule, it can influence the biological properties of the fusion protein. The relative merits of both approaches will become clear only after long-term laboratory and clinical testing, as their biological activity is also likely to differ. Given the clear differences in the mechanism of target molecule recognition, biochemical and biophysical properties (including molecular weight) and specificity, they cannot be considered as equivalent, unless extensive long-term clinical studies prove otherwise.

Endometrial carcinoma is among the most frequently diagnosed gynecological malignancies in highly developed countries. Research has been conducted for 20 years to define the molecular pathology of this disease and much is already known, but adequate prognostic, diagnostic, and monitoring markers are still missing. Recently, mitochondrial research opened a new perspective. The participation of abnormalities of those organelles and mutations of the mitochondrial genome has been defined in some types of cancer and is still under investigation. MtDNA mutations are also found in endometrial adenocarcinoma, although their impact on cell physiology has not been determined so far. Some processes involving mitochondria are widely known and described in numerous papers. These include electron transport and apoptosis, but others await further research. A forward genetics approach has been used in a wide spectrum of projects in which cancer tissue samples were collected from subjects with defined diagnoses and metabolic abnormalities and mtDNA mutations were checked. Thanks to this approach, characteristic patterns of mitochondrial disruption have been assigned to specific types of cancer. This review focuses on the molecular characteristics of endometrial adenocarcinoma with special focus on mitochondrial abnormalities. Research on cancer molecular pathology in endometrial adenocarcinoma may lead to the development of specific screening and/or diagnostic markers.

Recently published papers report a large number of mitochondrial DNA mutations in many different cancer types, but their significance for electron transport chain proteins remains unknown. This review covers structural mutations of mitochondrial genes, choosing prostate cancer, esophageal cancer and epithelioma as research models. As all mitochondrial genes encode subunits of the electron transport chain, the review focuses on the consequences of structural mutations on cell metabolism.