PubMed · 4667319
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L Rutgeerts, G Tytgat, E Eggermont. 1972. Human enterokinase.. https://pubmed.ncbi.nlm.nih.gov/4667319/
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Marine picocyanobacteria of the genera Prochlorococcus and Synechococcus, the two most abundant phototrophs on Earth, thrive in oligotrophic oceanic regions. While it is well known that specific lineages are exquisitely adapted to prevailing in situ light and temperature regimes, much less is known of the molecular machinery required to facilitate occupancy of these low-nutrient environments. Here, we describe a hitherto unknown alkaline phosphatase, Psip1, that has a substantially higher affinity for phosphomonoesters than other well-known phosphatases like PhoA, PhoX, or PhoD and is restricted to clade III Synechococcus and a subset of high light I-adapted Prochlorococcus strains, suggesting niche specificity. We demonstrate that Psip1 has undergone convergent evolution with PhoX, requiring both iron and calcium for activity and likely possessing identical key residues around the active site, despite generally very low sequence homology. Interrogation of metagenomes and transcriptomes from TARA oceans and an Atlantic Meridional transect shows that psip1 is abundant and highly expressed in picocyanobacterial populations from the Mediterranean Sea and north Atlantic gyre, regions well recognized to be phosphorus (P)-deplete. Together, this identifies psip1 as an important oligotrophy-specific gene for P recycling in these organisms. Furthermore, psip1 is not restricted to picocyanobacteria and is abundant and highly transcribed in some α-proteobacteria and eukaryotic algae, suggesting that such a high-affinity phosphatase is important across the microbial taxonomic world to occupy low-P environments.
The amplified detection of a target DNA, based on the alkaline phosphatase oxidative hydrolysis of the soluble 5-bromo-4-chloro-3-indoyl phosphate to the insoluble indigo product as an amplification path, is addressed by two different sensing configurations. The accumulation of the insoluble product on Au electrodes or Au/quartz crystals alters the interfacial electron-transfer resistance at the Au electrode or the mass associated with the piezoelectric crystal, thus enabling the quantitative transduction of the DNA sensing by Faradaic impedance spectroscopy or microgravimetric quartz crystal microbalance measurements, respectively. One sensing configuration involves the association of a complex consisting of the target DNA and a biotinylated oligonucleotide to the functionalized transducers. The binding of the avidin/alkaline phosphatase conjugate to the sensing interface followed by the biocatalyzed precipitation provides the amplification path for the analysis of the target DNA. This analysis scheme was used to sense the target DNA with a sensitivity limit that corresponds to 5 x 10(-14) M. The second amplified detection scheme involves the use of a nucleic-acid-functionalized alkaline phosphatase as a biocatalytic conjugate for the precipitation of the insoluble product. Following this scheme, the functionalized transducers are interacted with the analyzed sample that was pretreated with the oligonucleotide-modified alkaline phosphatase, followed by the biocatalyzed precipitation as the amplification route for the analysis of the target DNA. By the use of this configuration, a detection limit corresponding to 5 x 10(-13) M was achieved. Real clinical samples of the Tay-Sachs genetic disorder were easily analyzed by the developed detection routes.
Activated T cells secrete multiple osteoclastogenic cytokines which play a major role in the bone destruction associated with rheumatoid arthritis. While the role of T cells in osteoclastogenesis has received much attention recently, the effect of T cells on osteoblast formation and activity is poorly defined. In this study, we investigated the hypothesis that in chronic inflammation activated T cells contribute to enhanced bone turnover by promoting osteoblastic differentiation. We show that T cells produce soluble factors that induce alkaline phosphatase activity in bone marrow stromal cells and elevated expression of mRNA for Runx2 and osteocalcin. This data indicate that T cell derived factors have the capacity to stimulate the differentiation of bone marrow stromal cells into the osteoblast phenotype. RANKL mRNA was undetectable under any conditions in highly purified bone marrow stromal cells. In contrast, RANKL was constitutively expressed in primary osteoblasts and only moderately up-regulated by activated T cell conditioned medium. Interestingly, both bone marrow stromal cells and osteoblasts expressed mRNA for RANK, which was strongly up-regulated in both cell types by activated T cell conditioned medium. Although, mRNA for the RANKL decoy receptor, osteoprotegerin, was also up-regulated by activated T cell conditioned medium, it's inhibitory effects may be mitigated by a simultaneous rise in the osteoprotegerin competitor TNF-related apoptosis-inducing ligand. Based on our data we propose that during chronic inflammation, T cells regulate bone loss by a dual mechanism involving both direct stimulation of osteoclastogenesis, by production of osteoclastogenic cytokines, and indirectly by induction of osteoblast differentiation and up-regulation of bone turnover via coupling.