Of the A. marina chromosome nucleotide sequence (vs. itself) shows 18.7 of the sequence (not including the original, duplicated sequence) has a homology of greater than E 1 10 10 to another location on the chromosome. This is significantly higher than the 11.2 and 5.8 duplication in Synechocystis PCC6803 and Nostoc sp. PCC7120, respectively. A. marina actually has far fewer duplicated regions t
Blasts, bone marrow mast cells, neutrophils, macrophages, and cardiac myocytes (140). Various triggers induce synthesis of ET-1 including TGF- and other growth factors, cold exposure, low shear stress, hypoxia, and angiotensin II (140); but its synthesis is reduced by nitric oxide (NO), natriuretic peptides, increased blood flow, and prostacyclinCD87 (UPAR)(141). ET-1 is also degraded by MMP-1, wh
Synthesis (Fig. 3). There is no clear differentiation that would explain the near-complete conversion of -carotene to zeaxanthin by -carotene hydroxylase (CrtR), the enzyme responsible for zeaxanthin biosynthesis. We suggest a putative carotene biosynthesis pathway (Fig. 3) that accommodates the distinct complement of the carotenoid biosynthesis enzymes and their end products in A. marina.Light-Ha
Synthesis (Fig. 3). There is no clear differentiation that would explain the near-complete conversion of -carotene to zeaxanthin by -carotene hydroxylase (CrtR), the enzyme responsible for zeaxanthin biosynthesis. We suggest a putative carotene biosynthesis pathway (Fig. 3) that accommodates the distinct complement of the carotenoid biosynthesis enzymes and their end products in A. marina.Light-Ha
Rently free to specialize their metabolic library.ATP Synthase. One interesting case of the idiosyncratic plasmidgene library in A. marina is the inclusion of a second full set of ATP synthase genes on plasmid pREB4 (AM1 D0157-67). These genes are arranged into a unique operon and the individual proteins do not clearly fit into any of the described families (SI Fig. 5) (25). This unusual operon is
Nd J.W.T. contributed new reagents/analytic tools; W.D.S., M.C., P.C.C., A.L.C., L.C.D., B.M.H., L.E.K., A.K., S.L., S.D.M., H.M., L.P., P.R., S.S., W.M.S., Y.S., H.L.T., T. Tomo, T. Tsuchiya, Z.T.W., and R.E.B. analyzed data; and W.D.S. and M.C. wrote the paper. The authors declare no conflict of interest. This article is a PNAS Direct Submission. Data deposition: The sequences reported in this p
Induced responses.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptConclusionsInfluenza infection triggers a robust B cell response in the lymphoid tissues of the respiratory tract that provides immune protection from both primary and secondary infections. The regulation of this B cell response highlights the complexities of humoral response induction and maintenance to re
Induced responses.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptConclusionsInfluenza infection triggers a robust B cell response in the lymphoid tissues of the respiratory tract that provides immune protection from both primary and secondary infections. The regulation of this B cell response highlights the complexities of humoral response induction and maintenance to re