摘要:

AbstractThe photoregulation of chloroplast development in pea leaves has been studied by reference to three polypeptides and their mRNAs. The polypeptides were the large subunit (LSU) and the small subunit (SSU) of ribulose 1,5‐bisphosphate carbox‐ylase/oxygenase (RUBISCO), and the light‐harvesting chlorophyll a/b protein (LHCP). The polypeptides were assayed by a sensitive radioimmune assay, and the mRNAs were assayed by hybridization to cloned DNA probes. LSU, LSU mRNA, and LHCP mRNA were detectable in etiolated seedlings but LHCP, SSU, and SSU mRNA were at or below the limit of detection. During the first 48 hr of de‐etiolation under continuous white light, the mRNAs for LSU, SSU, and LHCP increased in concentration per apical bud by about 40‐fold, at least 200‐fold, and about 25‐fold, respectively, while the total RNA content per apical bud increased only 3.5‐fold. In the same period, the LSU, SSU, and LHCP contents per bud increased at least 60‐, 100‐, and 200‐fold, respectively. The LHCP increased steadily in concentration during de‐etiolation, whereas the accumulation LSU, SSU, and SSU mRNA showed a 24‐hr lag. The accumulation of SSU, SSU mRNA, and LHCP mRNA showed classical red/far‐red reversibility, indicating the involvement of phytochrome in the regulatory mechanism. LSU and LSU mRNA were induced equally well by red and far‐red light. The LHCP failed to accumulate except under continuous illumination. These results indicate that the accumulation of SSU is controlled largely through the steady‐state level of its mRNA, which is in turn almost totally dependent on light as an inducer and on phytochrome as one of the photoreceptors. The accumulation of LSU is largely but not totally determined by the level of its mRNA, which appears to be under strong photoregulation, which has yet to be shown to involve phytochrome. Phytochrome is involved in the regulation of LHCP mRNA levels but substantial levels of the mRNA also occur in the dark. LHCP accumulation is not primarily governed by the levels of LHCP mRNA but by posttranslational stabilization in which chlorophyll synthesis plays a ne

ISSN:0730-2312    

DOI:10.1002/jcb.240250102

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractIt has previously been found that naphthoquinones can potentiate the rate of hydrogen peroxide production by mitochondrial preparations of Trypanosoma brucei brucei and that organisms treated with naphthoquinones are more susceptible to lysis, especially in the presence of compounds such as heme, which promote the homolytic cleavage of hydrogen peroxide. We have evaluated the lytic effect of various N‐substitutedp‐benzoquinone imines both in vitro and in vivo and have attempted to correlate their structure with trypanocidal activity using the Hansch approach. While none of the compounds tested proved to be active in vivo, all caused the lysis of trypanosomes in vitro. The parameters that correlated best with trypanocidal activity were the conditional redox potential, the lipophilicity of the substituent attached to the nitrogen atom and the number of active hydrogens on the quinoncid ring. These findings suggest two possible modes of action, which may in fact be related. Conjugate nucleophilic addition and/or oxidative damage could be responsible for lysis of the parasites. These same compounds were previously found to be active against the ascitic sarcoma 180 in mice. The strong correlation between antineoplastic activity in vivo and trypanocidal activity in vitro suggests a similar mode of action in both cases. Further studies aimed at developing a quinonelike compound that will be active against trypanosomes in vivo are now in progr

ISSN:0730-2312    

DOI:10.1002/jcb.240250103

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractAntibodies against pure discoidin I have been used as a tool to ascertain the role of this lectin in aggregation of Dictyostelium discoideum. Discoidin I is widely expressed over the cell surface of aggregation‐competent AX‐2 cells, as ascertained by indirect immunofluorescence with specific (antidiscoidin I) antibodies. Univalent antidiscoidin I antibodies (Fab fragments) inhibit the aggregation‐specific intercellular adhesion of D discoideum AX‐2 cells in an in vitro assay. This inhibition depends on antibody concentration and cell density; a 50% inhibition of cell aggregation was obtained at antidiscoidin I Fab concentration of 4.5 mg/ml and 1 × 106cells/ml. Aggregation and morphogenesis on solid support is also effectively inhibited when AX‐2 cells are starved in the presence of antidiscoidin I Fab fragments. The inhibition of morphogenesis is also dose dependent and more effective than in the in vitro assay. No inhibition of aggregation either in the in vitro assay or on morphogenesis on solid support was observed with preimmune Fab fragments at any of the concentrations tested (up to

ISSN:0730-2312    

DOI:10.1002/jcb.240250104

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

摘要:

AbstractThe suppression of antibody formation to sheep red cells in mice by partially purified fractions of mouse submaxillary gland [7] was shown to be caused by epidermal growth factor (EGF). Purification of EGF by the method of Savage and Cohen [11]resolved three components referred to as EGFa, EGFb, and EGFc.All three induced premature eye opening in neonatal mice, but only EGFa(identified as EGF1‐53) had full immunosuppressive activity. EGFcwas shown by micropeptide mapping of chymotryptic and thermolytic digests and aminoterminal analysis to differ from EGFaonly by the presence of β‐aspartyl instead of an asparaginyl residue. EGFbdiffered from EGFain that it lacked the N‐terminal asparagine. EGF shortened enzymatically at its carboxy terminal by two or five amino acids did not have any immunosuppressive activity. These findings‐suggest that, in contrast to some other biological effects of EGF, intact amino and carboxy terminals are required for the expression of immunosuppressive

ISSN:0730-2312    

DOI:10.1002/jcb.240250105

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY

ISSN:0730-2312    

DOI:10.1002/jcb.240250101

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1984

数据来源: WILEY