Abstract.-The chemical taxonomic relationship of microorganisms has been studied through the hydrocarbon fraction of their chemical constituents. The diagenesis and biological transformations of some hydrocarbons in sediments is suggested, as a result of this information.Various compounds of presumed biological origin have been isolated from petroleum,' ancient sediments,2-4 and meteorites.5 Among these classes of organic compounds, the hydrocarbons have probably received the most attention. Meinscheinr found that the extracts of soil contained more odd than even carbon-numbered normal paraffins. Bray' reported that the ratio of odd over even carbon-numbered n-paraffins is significant in Recent sediments, approximately 2.4 to 5.5. However, the value decreases for older sediments, and it is close to 1.0 in petroleum. The isoprenoid hydrocarbons with the regular headtail-head-tail linkage have been taken to be the residue of life forms.3Barghoorn and his co-workers8' 9 claimed to have found blue-green algae and bacterialike microfossils in Precambrian rocks. It is very important to obtain confirmatory evidence for the existence of these primitive microorganisms in the Precambrian period.Chemical criteria can be used as confirmatory evidence for classifying living organisms which were previously identified solely on the basis of morphologic characteristics. Chemistry may have more to contribute than any morphological analysis, not only because of the relative evanescence of most plant tissues in geological deposits, but also because the biochemistry of evolutionary processes may be deduced from the presence of compounds from known diagenic pathways.The evolutionary step from the procaryotic cell (blue-green algae and bacteria) to the eucaryotic cell (green algae, fungi, protozoa, higher plants, and animals) is recognized by the appearance (or presence, in some cases) of nuclear membrane, mitotic division, chromosome number, cytoplasmic streaming, and mitochondria in the eucaryotic cell. Since lipids are important constituents of cytoplasmic and intracellular membranes, chemical taxonomic studies have been made to determine whether such evolutionary transitions are reflected at the molecular level.

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Ferritin binds specifically and saturably to a variety of cell types, and recently several ferritin receptors have been cloned. TIM-2 is a specific receptor for H ferritin (HFt) in the mouse. TIM-2 is a member of the T cell immunoglobulin and mucin domain containing (TIM) protein family and plays an important role in immunity. The expression of TIM-2 outside of the immune system indicates that this receptor may have broader roles. We tested whether ferritin binding to TIM-2 can serve as an iron delivery mechanism. TIM-2 was transfected into normal (TCMK-1) mouse kidney cells, where it was appropriately expressed on the cell surface. HFt was labeled with 55Fe and 55Fe-HFt was incubated with TIM-2 positive cells or controls. 55Fe-HFt uptake was observed only in TIM-2 positive cells. HFt uptake was also seen in A20 B cells, which express endogenous TIM-2. TIM-2 levels were not increased by iron chelation. Uptake of 55Fe-HFt was specific and temperature-dependent. HFt taken up by TIM-2 positive cells transited through the endosome and eventually entered a lysosomal compartment, distinguishing the HFt pathway from that of transferrin, the classical vehicle for cellular iron delivery. Iron delivered following binding of HFt to TIM-2 entered the cytosol and became metabolically available, resulting in increased levels of endogenous intracellular ferritin. We conclude that TIM-2 can function as an iron uptake pathway.

Signaling via the NF-κB cascade is critical for innate recognition of microbial products and immunity to infection. As a consequence, this pathway represents a strong selective pressure on infectious agents and many parasitic, bacterial and viral pathogens have evolved ways to subvert NF-κB signaling to promote their survival. Although the mechanisms utilized by microorganisms to modulate NF-κB signaling are diverse, a common theme is targeting of the steps that lead to IκB degradation, a major regulatory checkpoint of this pathway. The data presented here demonstrate that infection of mammalian cells with Toxoplasma gondii results in the activation of IKK and degradation of IκB. However, despite initiation of these hallmarks of NF-κB signaling, neither nuclear accumulation of NF-κB nor NF-κB-driven gene expression is observed in infected cells. However, this defect was not due to a parasite-mediated block in nuclear import, as general nuclear import and constitutive nuclear-cytoplasmic shuttling of NF-κB remain intact in infected cells. Rather, in T. gondii-infected cells, the termination of NF-κB signaling is associated with reduced phosphorylation of p65/RelA, an event involved in the ability of NF-κB to translocate to the nucleus and bind DNA. Thus, these studies demonstrate for the first time that the phosphorylation of p65/RelA represents an event downstream of IκB degradation that may be targeted by pathogens to subvert NF-κB signaling.