THE SULFUR-OXIDIZING PROKARYOTESBiological oxidation of hydrogen sulfide to sulfate is one of the major reactions of the global sulfur cycle. Reduced inorganic sulfur compounds (referred to below as sulfur) are exclusively oxidized by prokaryotes, and sulfate is the major oxidation product. Sulfur oxidation in members of the Eukarya is mediated by lithoautotrophic bacterial endosymbionts (44).The sulfur-oxidizing prokaryotes are phylogenetically diverse ( Fig. 1). In the domain Archaea aerobic sulfur oxidation is restricted to members of the order Sulfolobales (21, 58), and in the domain Bacteria sulfur is oxidized by aerobic lithotrophs or by anaerobic phototrophs. The nonphototrophic obligate anaerobe Wolinella succinogenes oxidizes hydrogen sulfide to polysulfide during fumarate respiration (41). The ecology, physiology, and biochemistry of sulfur-oxidizing bacteria have been reviewed previously. The neutrophilic chemolithotrophic bacteria have been reviewed by Kelly et al. (31,32,35) and Takakuwa (63), the acidophilic sulfur-oxidizing bacteria have been reviewed by Harrison (23) and Pronk et al. (46), and the molecular genetics of Acidithiobacillus ferrooxidans has been reviewed by Rawlings and Kusano (49). The sulfur metabolism of phototrophic bacteria has been reviewed by Brune (9,10) and Trüper and Fischer (65). The physiology and genetics of both phototrophic and lithotrophic sulfur-oxidizing prokaryotes have been discussed recently (18).Prokaryotes oxidize hydrogen sulfide, sulfur, sulfite, thiosulfate, and various polythionates under alkaline (57), neutral, or acidic conditions (23). Aerobic sulfur-oxidizing prokaryotes belong to genera like
Quantitative AF imaging appears feasible. It may enhance understanding of retinal degeneration, serve as a diagnostic aid and as a sensitive marker of disease progression, and provide a tool to monitor the effects of therapeutic interventions.
Loss of heterozygosity (LOH) and in silico expression analysis were applied to identify genes significantly downregulated in breast cancer within the genomic interval 6q23-25. Systematic comparison of candidate EST sequences with genomic sequences from this interval revealed the genomic structure of a potential target gene on 6q24.3, which we called SAM and SH3 domain containing 1 (SASH1). Loss of the gene-internal marker D6S311, found in 30% of primary breast cancer, was significantly correlated with poor survival and increase in tumor size. Two SASH1 transcripts of approximately 4.4 and 7.5 kb exist and are predominantly transcribed in the human breast, lung, thyroid, spleen, placenta and thymus. In breast cancer cell lines, SASH1 is only expressed at low levels. SASH1 is downregulated in the majority (74%) of breast tumors in comparison with corresponding normal breast epithelial tissues. In addition, SASH1 is also downregulated in tumors of the lung and thyroid. Analysis of the protein domain structure revealed that SASH1 is a member of a recently described family of SH3/SAM adapter molecules and thus suggests a role in signaling pathways. We assume that SASH1 is a new tumor suppressor gene possibly involved in tumorigenesis of breast and other solid cancers. We were unable to find mutations in the coding region of the gene in primary breast cancers showing LOH within the critical region. We therefore hypothesize that other mechanisms as for instance methylation of the promoter region of SASH1 are responsible for the loss of expression of SASH1 in primary and metastatic breast cancer.
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