16 research outputs found
Transport by molecular motors in the presence of static defects
The transport by molecular motors along cytoskeletal filaments is studied
theoretically in the presence of static defects. The movements of single motors
are described as biased random walks along the filament as well as binding to
and unbinding from the filament. Three basic types of defects are
distinguished, which differ from normal filament sites only in one of the
motors' transition probabilities. Both stepping defects with a reduced
probability for forward steps and unbinding defects with an increased
probability for motor unbinding strongly reduce the velocities and the run
lengths of the motors with increasing defect density. For transport by single
motors, binding defects with a reduced probability for motor binding have a
relatively small effect on the transport properties. For cargo transport by
motors teams, binding defects also change the effective unbinding rate of the
cargo particles and are expected to have a stronger effect.Comment: 20 pages, latex, 7 figures, 1 tabl
A four kinetic state model of fast axonal transport: Model formulation and perturbation solution
Evidence for a role of the synaptonemal complex in provision for normal chromosome disjunction at meiosis II in maize
Characterization of the karyotype of proasellus meridianusby differential staining techniques
The genome of Proasellus meridianus (2 n= 10) contains two kinds of constitutive heterochromatin: one, polymorphic and stainable with Chromomycin A3 located on certain telomeres, and the other centromeric and stainable with Hoechst 33258, visible only at pachytene. The NORs stainable with silver nitrate are terminal and located on at least three pairs of chromosomes. In diakinesis and first meiotic metaphase, usually the silver technique differentially stains the centromeric area of only one of the two sister chromatids of each homologue. This indicates a direct relationship between silver staining and kinetochore function. Surface spread of testicular tissue displays five synaptonemal complexes which are homogeneous throughout their length
The lithic assemblage from Sugenya, a Pastoral Neolithic site of the Elmenteitan tradition in southwestern Kenya
Analytical solution of equations describing slow axonal transport based on the stop-and-go hypothesis
The Yeast Kinesin-related Protein Smy1p Exerts Its Effects on the Class V Myosin Myo2p via a Physical Interaction
Meiotic Cohesion Requires Accumulation of ORD on Chromosomes before Condensation
Cohesion between sister chromatids is a prerequisite for accurate chromosome segregation during mitosis and meiosis. To allow chromosome condensation during prophase, the connections that hold sister chromatids together must be maintained but still permit extensive chromatin compaction. In Drosophila, null mutations in the orientation disruptor (ord) gene lead to meiotic nondisjunction in males and females because cohesion is absent by the time that sister kinetochores make stable microtubule attachments. We provide evidence that ORD is concentrated within the extrachromosomal domains of the nuclei of Drosophila primary spermatocytes during early G2, but accumulates on the meiotic chromosomes by mid to late G2. Moreover, using fluorescence in situ hybridization to monitor cohesion directly, we show that cohesion defects first become detectable in ord(null) spermatocytes shortly after the time when wild-type ORD associates with the chromosomes. After condensation, ORD remains bound at the centromeres of wild-type spermatocytes and persists there until centromeric cohesion is released during anaphase II. Our results suggest that association of ORD with meiotic chromosomes during mid to late G2 is required to maintain sister-chromatid cohesion during prophase condensation and that retention of ORD at the centromeres after condensation ensures the maintenance of centromeric cohesion until anaphase II