scholarly journals DISTRIBUTIVE PAIRING: THE SIZE-DEPENDENT MECHANISM FOR REGULAR SEGREGATION OF THE FOURTH CHROMOSOMES IN DROSOPHILA MELANOGASTER

1964 ◽  
Vol 52 (2) ◽  
pp. 226-232 ◽  
Author(s):  
R. F. Grell
2012 ◽  
Vol 109 (50) ◽  
pp. 20485-20490 ◽  
Author(s):  
B. Kasmapour ◽  
A. Gronow ◽  
C. K. E. Bleck ◽  
W. Hong ◽  
M. G. Gutierrez

Genetics ◽  
1997 ◽  
Vol 146 (2) ◽  
pp. 447-456 ◽  
Author(s):  
Brandon A Mann ◽  
James M Slauch

The generalized transducing bacteriophage of Salmonella typhimurium, P22, can transduce plasmids in addition to chromosomal markers. Previous studies have concentrated on transduction of pBR322 by P22 and P22HT, the high transducing mutant of P22. This study investigates the mechanism of P22HT transduction of low-copy number plasmids, namely pSC101 derivatives. We show that P22HT transduces pSC101 derivatives that share homology with the chromosome by two distinct mechanisms. In the first mechanism, the plasmid integrates into the chromosome of the donor by homologous recombination. This chromosomal fragment is then packaged in the transducing particle. The second mechanism is a size-dependent mechanism involving a putative plasmid multimer. We propose that this multimer is formed by interplasmidic recombination. In contrast, P22HT can efficiently transduce pBR322 by a third mechanism, which is independent of plasmid homology with the chromosome. It has been proposed that the phage packages a linear concatemer created during rolling circle replication of pBR322, similar in fashion to phage genome packaging. This study investigates the role of RecA, RecD, and RecF recombination proteins in plasmid/plasmid and plasmid/chromosome interactions that form packageable substrates in the donor. We also examine the resolution of various transduced plasmid species in the recipient and the roles of RecA and RecD in these processes.


2020 ◽  
Author(s):  
Minsuk Kwak ◽  
Kaden M. Southard ◽  
Nam Hyeong Kim ◽  
Ramu Gopalappa ◽  
Woon Ryoung Kim ◽  
...  

Aberrant cleavage of Notch and amyloid precursor proteins (APPs) by γ-secretase is implicated in numerous diseases, but how cleavage is regulated in space and time is unclear. Here, we report that cadherin-based adherens junctions (cadAJs) are sites of high cell-surface γ-secretase activity, while simultaneously excluding these γ-secretase substrates by a size-dependent mechanism, prohibiting enzyme-substrate interactions. Upon activation, Notch and APP undergo drastic spatial rearrangements to cadAJs, concentrating them with γ-secretase, wherein they are further processed for downstream signaling. Spatial mutation by decreasing (or increasing) the size of Notch extracellular domain promotes (or inhibits) signaling, respectively. Dysregulation of this spatial switch also promotes formation of more amyloidogenic Aβ. Therefore, cadAJs creates distinct biochemical compartments regulating signaling events involving γ-secretase and prevent pathogenic activation of its substrates.


2019 ◽  
Author(s):  
Thomas R. Lerner ◽  
Christophe J. Queval ◽  
Rachel P. Lai ◽  
Matthew Russell ◽  
Antony Fearns ◽  
...  

AbstractThe ability of Mycobacterium tuberculosis to form serpentine cords is intrinsically related to its virulence, but specifically how M. tuberculosis cording contributes to pathogenesis remains obscure. We show that several M. tuberculosis clinical isolates form intracellular cords in primary human lymphatic endothelial cells (hLEC) in vitro and also in the lymph nodes of patients with tuberculosis. We identified via RNA-seq a transcriptional programme in hLEC that activates cellular pro-survival and cytosolic surveillance of intracellular pathogens pathways. Consistent with this, cytosolic access of hLEC is required for intracellular M. tuberculosis cording; and cord formation is dependent on the M. tuberculosis ESX-1 type VII secretion system and the mycobacterial lipid PDIM. Finally, we show that M. tuberculosis cording is a novel size-dependent mechanism used by the pathogen to evade xenophagy in the cytosol of endothelial cells. These results provide a mechanism that explains the long-standing association between M. tuberculosis cording and virulence.


2019 ◽  
Author(s):  
Alexandra Colin ◽  
Nitzan Razin ◽  
Maria Almonacid ◽  
Wylie Ahmed ◽  
Timo Betz ◽  
...  

AbstractThe mechanism for nucleus centering in mouse oocytes results from a gradient of actin-positive vesicles. By microinjecting oil droplets and fluorescent beads, we analyze the consequences of the gradient of activity on transport of exogenous tracer particles of different sizes. We also use optical tweezers to probe rheological properties of the cytoplasm. We find that the gradient activity induces a general centering force, akin to an effective pressure gradient, leading to centering of oil droplets with velocities comparable to nuclear ones. High temporal resolution measurements reveal that passive particles, larger than 1µm, experience the activity gradient by a biased diffusion towards the cell center. Unexpectedly, this general and size dependent mechanism is maintained in Meiosis I but contrasted by a further process that specifically off-centers the spindle. These antagonizing processes depend on myosin activity, thus we reconcile how the same molecular actors can have two opposite functions (centering versus off-centering).


Genetics ◽  
1972 ◽  
Vol 70 (4) ◽  
pp. 567-581
Author(s):  
Charleen M Moore ◽  
Rhoda F Grell

ABSTRACT The behavior of a compound metacentric fourth chromosome (see PDF) has been examined to determine whether arm length or total length is the basis for recognition in distributive pairing. Recognition was judged by the frequency with which the (see PDF) nondisjoined from a series of X duplications (Dp), ranging in size from ≤ 0.3 to > 4 times the size of a single fourth chromosome. Dp, (see PDF) nondisjunction was measured in the absence and in the presence of a competitor, a compound metacentric X. In both situations, total length and not arm length, was found to confer the characteristic recognition property to the (see PDF). A comparison of Dp, (see PDF) nondisjunction curves for both the noncompetitive and competitive situations with analogous Dp, 4 curves previously obtained, show the Dp, (see PDF) curves to be similar in shape to those obtained earlier but displaced one unit to the right, corresponding precisely to the difference in size between the (see PDF) and the 4. Rules governing chromosome recognition for acrocentrics were found completely applicable to metacentrics; disjunctive behavior of metacentrics differed from that of acrocentrics in that two arms conferred on a chromosome the capacity to act as the intermediate of a trivalent when size no longer warranted this attribute. This capacity, itself, is size-dependent.


Genetics ◽  
1987 ◽  
Vol 116 (3) ◽  
pp. 409-413
Author(s):  
Bruce McKee

ABSTRACT Males carrying certain X-4 translocations exhibit strongly skewed sperm recovery ratios. The XP4D half of the translocation disjoins regularly from the Y chromosome and the 4PXD half disjoins regularly from the normal 4. Yet the smaller member of each bivalent is recovered in excess of its pairing partner, apparently due to differential gametic lethality. Chromosome recovery probabilities are multiplicative; the viability of each genotype is the product of the recovery probability of its component chromosomes. Meiotic drive can also be caused by deficiency for X heterochromatin. In(1)sc4Lsc8R males show the same size dependent chromosome recoveries and multiplicative recovery probabilities found in T(1;4)BS males. Meiotic drive in In(1)sc4Lsc8R males has been shown to be due to X-Y pairing failure. Although pairing is regular in the T(X;4) males, the striking phenotypic parallels suggest a common explanation. The experiments described below show that the two phenomena are, in fact, one and the same. X-4 translocations are shown to have the same effect on recovery of independently assorting chromosomes as does In(1)sc4Lsc8R. Addition of pairing sites to the 4PXD half of the translocation eliminates drive. A common explanation—failure of the distal euchromatic portion of the X chromosome to participate in X:Y meiotic pairing—is suggested as the cause for drive. The effect of X chromosome breakpoint on X-4 translocation induced meiotic drive is investigated. It is found that translocations with breakpoints distal to 13C on the salivary map do not cause drive while translocations broken proximal to 13C cause drive. The level of drive is related to the position of the breakpoint—the more proximal the breakpoint the greater the drive.


2020 ◽  
Author(s):  
Gesa F. Dinges ◽  
Alexander S. Chockley ◽  
Till Bockemühl ◽  
Kei Ito ◽  
Alexander Blanke ◽  
...  

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