Magnetic analyses of ODP Hole 119-738B sediments

Magnetotactic bacteria intracellularly biomineralize magnetite of an ideal grain size for recording palaeomagnetic signals. However, bacterial magnetite has only been reported in a few pre-Quaternary records because progressive burial into anoxic diagenetic environments causes its dissolution. Deep-sea carbonate sequences provide optimal environments for preserving bacterial magnetite due to low rates of organic carbon burial and expanded pore-water redox zonations. Such sequences often do not become anoxic for tens to hundreds of metres below the seafloor. Nevertheless, the biogeochemical factors that control magnetotactic bacterial populations in such settings are not well known. We document the preservation of bacterial magnetite, which dominates the palaeomagnetic signal throughout Eocene pelagic carbonates from the southern Kerguelen Plateau, Southern Ocean. We provide evidence that iron fertilization, associated with increased aeolian dust flux, resulted in surface water eutrophication in the late Eocene that controlled bacterial magnetite abundance via export of organic carbon to the seafloor. Increased flux of aeolian iron-bearing phases also delivered iron to the seafloor, some of which became bioavailable through iron reduction. Our results suggest that magnetotactic bacterial populations in pelagic settings depend crucially on particulate iron and organic carbon delivery to the seafloor.

Transactivation-deficient p73 alpha (p73 Delta exon2) inhibits apoptosis and competes with p53

p73 has recently been identified as a structural and functional homolog of the tumor suppressor protein p53. Overexpression of p53 activates transcription of p53 effector genes, causes growth inhibition and induced apoptosis. We describe here the effects of a tumor-derived truncated transcript of p73 alpha (p73 Delta exon2) on p53 function and on cell death. This transcript, which lacks the acidic N-terminus corresponding to the transactivation domain of p53, was initially detected in a neuroblastoma cell line. Overexpression of p73 Delta exon2 partially protects lymphoblastoid cells against apoptosis induced by anti-Fas antibody or cisplatin. By cotransfecting p73 Delta exon2 with wild-type p53 in the p53 null line Saos 2, we found that this truncated transcript reduces the ability of wild-type p53 to promote apoptosis. This anti-apoptotic effect was also observed when p73 Delta exon2 was co-transfected with full-length p73 (p73 alpha). This was further substantiated by suppression of p53 transactivation of the effector gene p21-Waf1 in p73 Delta exon2 transfected cells and by inhibition of expression of a reporter gene under the control of the p53 promoter. Thus, this truncated form of p73 can act as a dominant-negative agent towards transactivation by p53 and p73 alpha, highlighting the potential implications of these findings for p53 signaling pathway. Furthermore, we demonstrate the existence of a p73 Delta exon2 transcript in a very significant proportion (46%) of breast cancer cell lines. However, a large spectrum of normal and malignant tissues need to be surveyed to determine whether this transdominant p73 variant occurs in a tumor-specific manner.