排序方式: 共有40条查询结果,搜索用时 562 毫秒
1.
2.
The effect of lincocin (a plastid protein synthesis inhibitor) treatment on the greening process of bean (Phaseolus vulgaris L.) leaves have been studied. In comparison with control leaves treated ones had a decreased rate of chloroplast development. They had a marked chlorophyll deficiency and a decreased chlorophyll a/b ratio. Some long and short wavelength forms of chlorophyll a were lacking as evidenced from the absorption spectra at 25°C and the fluorescence spectra at 77°K. The –14CO2 fixation was inhibited by 80–90% in treated leaves. The fluorescence induced by the measuring light was greater in the treated leaves than in the control ones, and the kinetics of the decline of the relative fluorescence intensity were also different. Electron microscopic studies showed macrogranum-like structures and incomplete membrane vesicles in the treated plastids. After longer treatment a destruction of membranes was observed. The results indicate some structural and functional membrane deficiencies and instability of the membranes. 相似文献
3.
DIDIER FOURGON IGOR EECKHAUT DEVARAJEN VAÏTILINGON MICHEL JANGOUX 《Invertebrate reproduction & development.》2013,57(3):155-165
Summary The larval development of the ophiocomid ophiuroid Ophiomastix venosais described using SEM. The gastrula transforms into a uniformly ciliated early larva which progressively changes into a lecithotrophic late premetamorphic larva with a continuous bilateral ciliated band. This stage is short-lived and equivalent to a highly reduced ophiopluteus. Comparisons between O. venosa and other ophiuroid species whose development has been investigated suggest that, whatever the developmental mode (lecithotrophic or planktotrophic), a pluteus stage always occurs in ophiuroids with planktonic development. Two metamorphic stages were identified, the late metamorphic larva differing from the early one by the closure of the larval mouth. The appearance of the permanent mouth marks the end of the metamorphosis. The postlarva still possesses remnants of larval features. The transformation of the reduced ophiopluteus into a barrel-shaped metamorphic larva with transverse ciliated bands, a vitellaria larva, is followed. The possible occurrence of a unique type of metamorphic larva in non-brooding ophiuroids is discussed. Verification of this, however, needs further SEM investigations on metamorphic larva from species having “regular” planktotrophic development. 相似文献
4.
5.
6.
7.
In eukaryotic cells, Flap endonuclease 1 (FEN1) is a major structure-specific endonuclease that processes 5’ flapped structures during maturation of lagging strand DNA synthesis, long patch base excision repair, and rescue of stalled replication forks. Here we report that fanconi anemia complementation group A protein (FANCA), a protein that recognizes 5’ flap structures and is involved in DNA repair and maintenance of replication forks, constantly stimulates FEN1-mediated incision of both DNA and RNA flaps. Kinetic analyses indicate that FANCA stimulates FEN1 by increasing the turnover rate of FEN1 and altering its substrate affinity. More importantly, six pathogenic FANCA mutants are significantly less efficient than the wild-type at stimulating FEN1 endonuclease activity, implicating that regulation of FEN1 by FANCA contributes to the maintenance of genomic stability. 相似文献
8.
9.
Elena Sotillo Judit Garriga Amol Padgaonkar Alison Kurimchak Jeanette Gowen Cook Xavier Gra?a 《The Journal of biological chemistry》2009,284(21):14126-14135
We have previously shown that SV40 small t antigen (st) cooperates with
deregulated cyclin E to activate CDK2 and bypass quiescence in normal human
fibroblasts (NHF). Here we show that st expression in serum-starved and
density-arrested NHF specifically induces up-regulation and loading of CDC6
onto chromatin. Coexpression of cyclin E results in further accumulation of
CDC6 onto chromatin concomitantly with phosphorylation of CDK2 on Thr-160 and
CDC6 on Ser-54. Investigation of the mechanism leading to CDC6 accumulation
and chromatin loading indicates that st is a potent inducer of cdc6
mRNA expression and increases CDC6 protein stability. We also show that CDC6
expression in quiescent NHF efficiently promotes cyclin E loading onto
chromatin, but it is not sufficient to activate CDK2. Moreover, we show that
CDC6 expression is linked to phosphorylation of the activating T loop of CDK2
in serum-starved NHF stimulated with mitogens or ectopically expressing cyclin
E and st. Our data suggest a model where the combination of st and deregulated
cyclin E result in cooperative and coordinated activation of both an essential
origin licensing factor, CDC6, and an activity required for origin firing,
CDK2, resulting in progression from quiescence to S phase.Upon mitogenic stimulation mammalian G1
CDKs4 trigger passage
through the restriction point and the transition into DNA replication. In
particular, cyclin E/CDK2 is activated in mid to late G1 and phosphorylates a
variety of substrates that play critical roles in these processes. CDK2
cooperates with D-type cyclin/CDKs to inactivate E2F/pocket protein repressor
complexes inducing the expression of DNA synthesis factors and other cell
cycle regulators (reviewed in Refs.
1 and
2). CDK2 also phosphorylates
DNA replication factors facilitating prereplication complex assembly and
origin firing and plays additional roles in centrosome duplication and histone
synthesis (reviewed in Ref. 1).
In particular, it has been proposed that CDK2 phosphorylates the essential
origin licensing factor CDC6 promoting its stabilization prior to inactivation
of the APCCdh1 ubiquitin ligase
(3). This is thought to ensure
that CDC6 accumulation precedes accumulation of other APC substrates that
inhibit origin licensing. Moreover, CDK2-independent cyclin E functions have
also been reported to be important for prereplication complex assembly in
cells in transit from G0 into G1
(4,
5). In keeping with its role as
positive regulator of major G1 transitions, deregulation of the cyclin E via
gene amplification or defective protein turnover is commonly seen in primary
tumors and is associated with poor prognosis
(6–8).
In normal fibroblasts, ectopic expression of cyclin E has been associated with
shortening of the G1 phase of the cell cycle
(9,
10), and with induction of DNA
damage (reviewed in Ref. 8).
Cyclin E deregulation in certain human tumor cell lines and immortalized rat
fibroblasts is associated with mitogen-independent cell cycle entry and
progression through the cell cycle
(11). However, when cyclin E
is ectopically expressed in quiescent normal human fibroblasts (NHF), cells
remain in G0 (12).We have recently reported that coexpression of SV40 small t antigen (st) in
quiescent NHF with deregulated cyclin E expression is sufficient to trigger
mitogen-independent cell cycle progression, proliferation beyond cell
confluence, and foci formation. The bypass of quiescence induced by
the expression of st and cyclin E is dependent on CDK2 activation
(12). Thus, contrary to what
is seen in normal murine cells
(13), CDK2 activity appears
essential for cell cycle progression when it is oncogenically driven by cyclin
E and st expression (12).
Because st is known to target pathways uniquely required for the
transformation of human cells
(14,
15), tumor cells with altered
pathways that mimic st/cyclin E expression could predictably be sensitive to
selective inhibition of CDK2 activity.Given the critical role of CDK2 activity in cyclin E and st cooperation in
inducing cell proliferation and transformation of NHF, we sought to determine
the factors and mechanisms by which st modulates CDK2 activation. In this
report we have identified the CDC6 replication licensing factor as a cellular
target of st. We also uncover CDC6 as a participant in the events leading to
chromatin association of cyclin E and CDK2 and in phosphorylation of CDK2 on
its activating T loop both in response to mitogenic stimulation, as well as
expression of cyclin E and st in NHF. 相似文献
10.
Acceptor specificity of the human leukocyte alpha3 fucosyltransferase: role of FucT-VII in the generation of selectin ligands 总被引:2,自引:2,他引:0
Britten CJ; van den Eijnden DH; McDowell W; Kelly VA; Witham SJ; Edbrooke MR; Bird MI; de Vries T; Smithers N 《Glycobiology》1998,8(4):321-327
The alpha3 fucosyltransferase, FucT-VII, is one of the key
glycosyltransferases involved in the biosynthesis of the sialyl Lewis X
(sLex) antigen on human leukocytes. The sialyl Lewis X antigen
(NeuAcalpha(2-3)Galbeta(1-4)[Fucalpha(1-3)]GlcNAc-R) is an essential
component of the recruitment of leukocytes to sites of inflammation,
mediating the primary interaction between circulating leukocytes and
activated endothelium. In order to characterize the enzymatic properties of
the leukocyte alpha3 fucosyltransferase FucT-VII, the enzyme has been
expressed in Trichoplusia ni insect cells. The enzyme is capable of
synthesizing both sLexand sialyl-dimeric-Lexstructures in vitro , from
3'-sialyl-lacNAc and VIM-2 structures, respectively, with only low levels
of fucose transfer observed to neutral or 3'-sulfated acceptors. Studies
using fucosylated NeuAcalpha(2-3)-(Galbeta(1- 4)GlcNAc)3-Me acceptors
demonstrate that FucT-VII is able to synthesize both di-fucosylated and
tri-fucosylated structures from mono- fucosylated precursors, but
preferentially fucosylates the distal GlcNAc within a polylactosamine
chain. Furthermore, the rate of fucosylation of the internal GlcNAc
residues is reduced once fucose has been added to the distal GlcNAc. These
results indicate that FucT-VII is capable of generating complex selectin
ligands, in vitro , however the order of fucose addition to the lactosamine
chain affects the rate of selectin ligand synthesis.
相似文献