Gender Specific Reproductive Strategies of an Arctic Key Species (Boreogadus saida) and Implications of Climate Change

The Arctic climate is changing at an unprecedented rate. What consequences this may have on the Arctic marine ecosystem depends to a large degree on how its species will respond both directly to elevated temperatures and more indirectly through ecological interactions. But despite an alarming recent warming of the Arctic with accompanying sea ice loss, reports evaluating ecological impacts of climate change in the Arctic remain sparse. Here, based upon a large-scale field study, we present basic new knowledge regarding the life history traits for one of the most important species in the entire Arctic, the polar cod (Boreogadus saida). Furthermore, by comparing regions of contrasting climatic influence (domains), we present evidence as to how its growth and reproductive success is impaired in the warmer of the two domains. As the future Arctic is predicted to resemble today''s Atlantic domains, we forecast changes in growth and life history characteristics of polar cod that will lead to alteration of its role as an Arctic keystone species. This will in turn affect community dynamics and energy transfer in the entire Arctic food chain.     

Tumourigenesis Driven by the Human Papillomavirus Type 16 Asian-American E6 Variant in a Three-Dimensional Keratinocyte Model

Infection with a transforming human papillomavirus (HPV) such as type 16 (of species Alphapapillomavirus 9) causes ano-genital and oral tumours via viral persistence in human squamous cell epithelia. Epidemiological studies showed that the naturally occurring HPV16 Asian-American (AA) variant (sublineage D2/D3) is found more often than the European Prototype (EP) (sublineage A1) in high-grade cervical neoplasia and tumours compared to non-cancer controls. Just three amino acid changes within the early gene, E6, of HPV16 AA have been linked to this augmented tumourigenicity. The AAE6 variant''s greater immortalizing and transforming potential over EPE6 has recently been confirmed in retrovirally-transduced keratinocytes expressing the E6 gene only. However, the tumourigenic role of the full-length viral genome of HPV16 has not yet been addressed with regard to these E6 variants. To investigate this process in the context of these two HPV16 E6 genotypes, an organotypic tissue culture model was used to simulate the HPV infectious life cycle. The AAE6 variant demonstrated an enhanced ability over EPE6 to drive the viral life cycle toward tumourigenesis, as evidenced phenotypically—by a more severe grade of epithelial dysplasia with higher proliferation and deregulated differentiation, and molecularly—by high viral oncogene E6 and E7 expression, but lack of productive viral life cycle markers. In contrast, EPE6 had low E6 and E7 but high E1∧E4 expression, indicative of a productive life cycle. We suggest increased viral integration into the host genome for AAE6 as one possible mechanism for these observed differences from EPE6. Additionally, we found downstream effects on immortalization and host innate immune evasion. This study highlights how minor genomic variations in transforming viruses can have a significant affect on their tumourigenic ability.     

ALS‐associated fused in sarcoma (FUS) mutations disrupt Transportin‐mediated nuclear import

Mutations in fused in sarcoma (FUS) are a cause of familial amyotrophic lateral sclerosis (fALS). Patients carrying point mutations in the C‐terminus of FUS show neuronal cytoplasmic FUS‐positive inclusions, whereas in healthy controls, FUS is predominantly nuclear. Cytoplasmic FUS inclusions have also been identified in a subset of frontotemporal lobar degeneration (FTLD‐FUS). We show that a non‐classical PY nuclear localization signal (NLS) in the C‐terminus of FUS is necessary for nuclear import. The majority of fALS‐associated mutations occur within the NLS and impair nuclear import to a degree that correlates with the age of disease onset. This presents the first case of disease‐causing mutations within a PY‐NLS. Nuclear import of FUS is dependent on Transportin, and interference with this transport pathway leads to cytoplasmic redistribution and recruitment of FUS into stress granules. Moreover, proteins known to be stress granule markers co‐deposit with inclusions in fALS and FTLD‐FUS patients, implicating stress granule formation in the pathogenesis of these diseases. We propose that two pathological hits, namely nuclear import defects and cellular stress, are involved in the pathogenesis of FUS‐opathies.     

Resistenzverhalten einiger Maissorten und -hybriden auf künstlich erzeugte Kolbenmykosen unter Berücksichtigung der im Bernburger Raum häufig an Maiskolben auftretenden Pilzflora

Ohne ZusammenfassungHerrn Prof. Dr. Dr. h. c.H. Stubbe zum 60. Geburtstag gewidmet.     

Untersuchungen zur vitalen Fluorochromierung pflanzlicher Zellen mit Neutralrot

Ohne ZusammenfassungDer Deutschen Forschungsgemeinschaft danken wir für die Unterstützung unserer Arbeiten. Ferner danken wir Frau Ingeborg v. Tippelskirch und Fräulein Annemarie Pagels für ihre Hilfe.