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51.
A meiotic uv-sensitive mutant that causes deletion of duplications in neurospora 总被引:2,自引:1,他引:1 下载免费PDF全文
The meiotic-3 (mei-3) mutant of Neurospora crassa has several effects: (1) When homozygous, it almost completely blocks meiosis and ascospore formation, (2) it is sensitive to UV, (3) its growth is inhibited by histidine and, (4) it increases the instability of nontandem duplications. This was shown for duplications produced by five different rearrangements and was demonstrated by two different criteria. The effects on meiosis and duplication instability are expressed strongly at 25°; the effects on sensitivity to UV and to histidine are expressed strongly at 38.5° but only slightly at 25°. Nevertheless, all four effects were shown to be due to a single gene. mei-3 is not allelic with previously reported UV-sensitive mutants.—Two other results were obtained that are not necessarily due to mei-3: (1) A cross involving mei-3 produced a new unlinked meiotic mutant, mei-4, which is not sensitive to UV or histidine, and (2) a burst of several new mutants occurred in a different mei-3 stock, including a partial revertant of mei-3.—mei-3 has previously been shown to cause frequent complete loss of a terminal duplicate segment, beginning exactly at the original rearrangement breakpoint. Possible mechanisms are discussed by which a UV-sensitive mutant could cause such precise deletions. 相似文献
52.
A comparison of two methods for constructing evolutionary distances from a weighted contribution of transition and transversion differences 总被引:3,自引:3,他引:0
Since the initial work of Jukes and Cantor (1969), a number of procedures
have been developed to estimate the expected number of nucleotide
substitutions corresponding to a given observed level of nucleotide
differentiation assuming particular evolutionary models. Unlike the
proportion of different sites, the expected number of substitutions that
would have occurred grows linearly with time and therefore has had great
appeal as an evolutionary distance. Recently, however, a number of authors
have tried to develop improved statistical approaches for generating and
evaluating evolutionary distances (Schoniger and von Haeseler 1993;
Goldstein and Polock 1994; Tajima and Takezaki 1994). These studies clearly
show that the estimated number of nucleotide substitutions is generally not
the best estimator for use in reconstruction of phylogenetic relationships.
The reason for this is that there is often a large error associated with
the estimation of this number. Therefore, even though its expectation is
correct (i.e., on average the expected number of substitutions is
proportional to time- -but see Tajima 1993), it is not expected to be as
useful as estimators designed to have a lower variance.
相似文献
53.
WJ Richardson DD van der Voort E Wilson JE Moore Jr. 《Molecular & cellular biomechanics : MCB》2013,10(3):245-265
Non-uniform stress and strain fields are prevalent in many tissues in vivo, and often exacerbated by disease or injury. These mechanical gradients potentially play a role in contributing to pathological conditions, presenting a need for experimental tools to allow investigation of cell behavior within non-uniformly stimulated environments. Herein, we employ two in vitro cell-stretching devices (one previously published; one newly presented) capable of subjecting cells to cyclic, non-uniform stretches upon the surface of either a circular elastomeric membrane or a cylindrical PDMS tube. After 24 hours of cyclic stretch, 10T1/2 cells on both devices showed marked changes in long-axis orientation, with tendencies to align parallel to the direction of minimal deformation. The degree of this response varied depending on location within the stretch gradients. These results demonstrated the feasibility of conducting cell mechanobiology investigations with the two novel devices, while also highlighting the experimental capabilities of non-uniform mechanical environments for these types of studies. Such capabilities include robust data collection for developing mechanobiological dose-response curves, signal threshold identification, and potential spatial targeting for drug delivery. 相似文献
54.
55.
Laura A Gillies Han Du Bjoern Peters C. Michael Knudson Donald D. Newmeyer Tomomi Kuwana 《Molecular biology of the cell》2015,26(2):339-349
Bax induces mitochondrial outer membrane permeabilization (MOMP), a critical step in apoptosis in which proteins are released into the cytoplasm. To resolve aspects of the mechanism, we used cryo-electron microscopy (cryo-EM) to visualize Bax-induced pores in purified mitochondrial outer membranes (MOMs). We observed solitary pores that exhibited negative curvature at their edges. Over time, the pores grew to ∼100–160 nm in diameter after 60–90 min, with some pores measuring more than 300 nm. We confirmed these results using flow cytometry, which we used to monitor the release of fluorescent dextrans from isolated MOM vesicles. The dextran molecules were released gradually, in a manner constrained by pore size. However, the release rates were consistent over a range of dextran sizes (10–500 kDa). We concluded that the pores were not static but widened dramatically to release molecules of different sizes. Taken together, the data from cryo-EM and flow cytometry argue that Bax promotes MOMP by inducing the formation of large, growing pores through a mechanism involving membrane-curvature stress. 相似文献
56.
The pro-apoptotic proteins, Bid and Bax, cause a limited permeabilization of the mitochondrial outer membrane that is enhanced by cytosol 下载免费PDF全文
Kluck RM Esposti MD Perkins G Renken C Kuwana T Bossy-Wetzel E Goldberg M Allen T Barber MJ Green DR Newmeyer DD 《The Journal of cell biology》1999,147(4):809-822
During apoptosis, an important pathway leading to caspase activation involves the release of cytochrome c from the intermembrane space of mitochondria. Using a cell-free system based on Xenopus egg extracts, we examined changes in the outer mitochondrial membrane accompanying cytochrome c efflux. The pro-apoptotic proteins, Bid and Bax, as well as factors present in Xenopus egg cytosol, each induced cytochrome c release when incubated with isolated mitochondria. These factors caused a permeabilization of the outer membrane that allowed the corelease of multiple intermembrane space proteins: cytochrome c, adenylate kinase and sulfite oxidase. The efflux process is thus nonspecific. None of the cytochrome c-releasing factors caused detectable mitochondrial swelling, arguing that matrix swelling is not required for outer membrane permeability in this system. Bid and Bax caused complete release of cytochrome c but only a limited permeabilization of the outer membrane, as measured by the accessibility of inner membrane-associated respiratory complexes III and IV to exogenously added cytochrome c. However, outer membrane permeability was strikingly increased by a macromolecular cytosolic factor, termed PEF (permeability enhancing factor). We hypothesize that PEF activity could help determine whether cells can recover from mitochondrial cytochrome c release. 相似文献
57.
Yamaguchi R Lartigue L Perkins G Scott RT Dixit A Kushnareva Y Kuwana T Ellisman MH Newmeyer DD 《Molecular cell》2008,31(4):557-569
Controversy surrounds the role and mechanism of mitochondrial cristae remodeling in apoptosis. Here we show that the proapoptotic BH3-only proteins Bid and Bim induced full cytochrome c release but only a subtle alteration of crista junctions, which involved the disassembly of Opa1 complexes. Both mitochondrial outer membrane permeabilization (MOMP) and crista junction opening (CJO) were caspase independent and required a functional BH3 domain and Bax/Bak. However, MOMP and CJO were experimentally separable. Pharmacological blockade of MOMP did not prevent Opa1 disassembly and CJO; moreover, expression of a disassembly-resistant mutant Opa1 (Q297V) blocked cytochrome c release and apoptosis but not Bax activation. Thus, apoptosis requires a subtle form of Opa1-dependent crista remodeling that is induced by BH3-only proteins and Bax/Bak but independent of MOMP. 相似文献
58.
59.
BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly 总被引:13,自引:0,他引:13
Kuwana T Bouchier-Hayes L Chipuk JE Bonzon C Sullivan BA Green DR Newmeyer DD 《Molecular cell》2005,17(4):525-535
Using a Bax-dependent membrane-permeabilization assay, we show that peptides corresponding to the BH3 domains of Bcl-2 family "BH3-only" proteins have dual functions. Several BH3 peptides relieved the inhibition of Bax caused by the antiapoptotic Bcl-x(L) and/or Mcl-1 proteins, some displaying a specificity for either Bcl-x(L) or Mcl-1. Besides having this derepression function, the Bid and Bim peptides activated Bax directly and were the only BH3 peptides tested that could potently induce cytochrome c release from mitochondria in cultured cells. Furthermore, Bax activator molecules (cleaved Bid protein and the Bim BH3 peptide) synergistically induced cytochrome c release when introduced into cells along with derepressor BH3 peptides. These observations support a unified model of BH3 domain function, encompassing both positive and negative regulation of other Bcl-2 family members. In this model, the simple inhibition of antiapoptotic functions is insufficient to induce apoptosis unless a direct activator of Bax or Bak is present. 相似文献
60.
Bcl-2-family proteins and the role of mitochondria in apoptosis 总被引:31,自引:0,他引:31
Mitochondria are central to many forms of cell death, usually via the release of pro-apoptotic proteins from the mitochondrial intermembrane space. Some intermembrane space proteins, including cytochrome c, Smac/DIABLO, and Omi/Htra2, can induce or enhance caspase activation, whereas others, such as AIF and endonuclease G, might act in a caspase-independent manner. Intermembrane space protein release is often regulated by Bcl-2-family proteins. Recent evidence suggests that pro-apoptotic members of this family, by themselves, can permeabilize the outer mitochondrial membrane without otherwise damaging mitochondria. Mitochondria can contribute to cell death in other ways. For example, they can respond to calcium release from the endoplasmic reticulum by undergoing the mitochondrial permeability transition, which in turn causes outer membrane rupture and the release of intermembrane space proteins. Bcl-2-family proteins can influence the levels of releasable Ca(2+) in the endoplasmic reticulum, and thus determine whether the released Ca(2+) is sufficient to overload mitochondria and induce cell death. 相似文献