A novel photosynthetic strategy for adaptation to low-iron aquatic environments.

Iron (Fe) availability is a major limiting factor for primary production in aquatic environments. Cyanobacteria respond to Fe deficiency by derepressing the isiAB operon, which encodes the antenna protein IsiA and flavodoxin. At nanomolar Fe concentrations, a PSI-IsiA supercomplex forms, comprising a PSI trimer encircled by two complete IsiA rings.

Biospheric primary production during an ENSO transition.

The Sea-viewing Wide Field-of-view Sensor (SeaWiFS) provides global monthly measurements of both oceanic phytoplankton chlorophyll biomass and light harvesting by land plants. These measurements allowed the comparison of simultaneous ocean and land net primary production (NPP) responses to a major El Niño to La Niña transition. Between September 1997 and August 2000, biospheric NPP varied by 6 petagrams of carbon per year (from 111 to 117 petagrams of carbon per year).

Inhibition of development of murine melanoma lung metastases by systemic administration of recombinant platelet factor 4.

Background: When administered locally, recombinant platelet factor 4 (rPF4), a known angiogenesis inhibitor, has been shown to effectively suppress murine melanoma and human colon carcinoma primary tumor growth in mice. It was tentatively concluded that this effect was due to the inhibition of tumor neovascularization.

Purpose: This study has evaluated the effects of systemically administered rPF4 on the growth and establishment of experimental B16F10 melanoma lung metastases in syngeneic mice.

Induction of phorbol ester responsiveness in conventional B cells after activation via surface Ig.

The signals required to induce S phase entry in murine splenic B cells were found to be altered by prolonged treatment with low doses of anti-Ig antibody. Whereas fresh splenic B cells are stimulated by the combination of a phorbol ester protein kinase C agonist plus a calcium ionophore, anti-Ig-treated splenic B cells were stimulated by phorbol ester alone, in the absence of a comitogen. The majority of these phorbol ester responsive B cells expressed CD5.

Phorbol ester responsiveness of murine Ly-1-lineage B cells from normal and viable motheaten mutant mice.

Simultaneous analysis of stimulated cells for surface phenotype and DNA content by flow cytometry was used to delineate the characteristics of murine lymphocytes that respond to phorbol esters. Peritoneal cells that expressed high-density sIgM, Ly-1, Mac-1 and high-density Pgp-1, were preferentially stimulated to enter the S + G2/M phases of the cell cycle by the protein kinase C agonist, phorbol 12-myristate 13-acetate (PMA). Since these phenotypic characteristics correspond well with those of Ly-1-lineage B cells, non-peritoneal sources of Ly-1+ B cells were examined to test the relative role of lineage and environment in determining phorbol ester responsiveness.

Elevated expression of Pgp-1 (Ly-24) by murine peritoneal B lymphocytes.

B cell expression of the surface glycoprotein, Pgp-1 (Ly-24), was evaluated using flow cytometric analysis. Pgp-1 expression on naive, conventional (splenic) B cells was low but could be increased by mitogenic stimulation. Pgp-1 expression on naive peritoneal B cells was higher than expression by unmanipulated conventional B cells, suggesting the possibility that peritoneal B cells have been activated in vivo.

Anti-Ig antibody inhibits the phorbol ester-induced stimulation of peritoneal B cells.

Peritoneal B cells are stimulated to enter S phase by phorbol esters acting alone, in the absence of a co-mitogen. Anti-Ig antibody inhibited the stimulation of peritoneal B cells induced by phorbol esters and this inhibition was apparent throughout the time course of PMA-induced stimulation. Assessment of inhibition after depletion of Ly-1+ B cells suggested that PMA-induced stimulation of both Ly-1+ and Ly-1- B cells was affected by anti-Ig.

Peritoneal B cells respond to phorbol esters in the absence of co-mitogen.

B cells obtained by irrigation of the peritoneal cavity differ from splenic B cells in signaling requirements for the initiation of DNA synthesis. Splenic B cells are stimulated to enter S phase by phorbol esters in conjunction with a second signal provided by calcium ionophore; however, splenic B cells are not stimulated by phorbol ester alone. In contrast, peritoneal B cells from NZB and BALB/c mice were stimulated to incorporate tritiated thymidine by each of the phorbol esters, PMA and phorbol dibutyrate, acting alone.

Inhibition by phorbol esters of antiimmunoglobulin-induced calcium signalling and B-cell activation.

The inhibitory effect of phorbol dibutyrate (PDB) on B-cell stimulation was evaluated using a model in which activation is induced by modest doses of antiimmunoglobulin antibody (anti-Ig) and progression to DNA synthesis is induced by cytochalasin. PDB preferentially inhibited anti-Ig-induced activation and did so during brief (2 hr) preincubation with anti-Ig. Activation was inhibited whether PDB was added before or shortly after anti-Ig.

Stimulation of murine B cells by the combination of calcium ionophore plus phorbol ester.

The ability of calcium ionophore and phorbol ester to stimulate entry into S phase was assessed during short-term cultures of murine B cells extensively depleted of T cells. Neither ionomycin alone nor PMA alone stimulated DNA synthesis. However, the combination of ionomycin plus PMA acted in synergy to induce initiation of DNA synthesis in murine B cells.