Effect of the T-mutation on histogenesis of the mouse embryo under the testis capsule

Development ◽  
1979 ◽  
Vol 50 (1) ◽  
pp. 21-30
Author(s):  
H. Fujimoto ◽  
K. O. Yanagisawa
Keyword(s):  
Statistical Analysis ◽  
Bone Formation ◽  
Mouse Embryo ◽  
In Utero ◽  
Mouse Embryos ◽  
Wild Type ◽  
Germ Layers ◽  
Derivatives Of

Mouse embryos homozygous for the T-mutation show abnormalities, severer at the posterior embryonic regions, by day 9 of gestation and die before day 11 in utero. To analyse developmental potentiality of the T/T embryos, fragments of their anterior and posterior portions were grafted into the testes of adult T/+ mice, and examined histologically for the tissues formed after 1 month. The grafted tissues of the T/T embryos grew beyond the destined lethal stage and gave rise to benign teratomas composed of mature tissues. Although there were some different features of the tissues formed in the teratomas derived from different portions and stages of the embryos, their types were essentially identical between wild-type and the mutant teratomas. Statistical analysis showed that frequency of the cartilage and/or bone formation was significantly lower in the posterior mutant teratomas. It cannot be concluded, however, that this difference is essentially caused by T-mutation. The main conclusion of present experiments is that grafted portions of T/T embryos have the potentiality to develop intoteratomas containing derivatives of all three germ layers.

scholarly journals CHROMOSOMAL BASIS OF THE MEROZYGOSITY IN A PARTIALLY DIPLOID MUTANT OF PNEUMOCOCCUS

Genetics ◽  
1975 ◽  
Vol 80 (4) ◽  
pp. 667-678
Author(s):  
Mary Lee S Ledbetter ◽  
Rollin D Hotchkiss
Keyword(s):  
High Efficiency ◽  
Point Mutations ◽  
Resistant Mutant ◽  
Chromosomal Marker ◽  
Structural Abnormality ◽  
C Cells ◽  
Wild Type ◽  
Chromosomal Locus ◽  
Low Efficiency ◽  
Derivatives Of

ABSTRACT A sulfonamide-resistant mutant of pneumococcus, sulr-c, displays a genetic instability, regularly segregating to wild type. DNA extracts of derivatives of the strain possess transforming activities for both the mutant and wild-type alleles, establishing that the strain is a partial diploid. The linkage of sulr-c to strr-61, a stable chromosomal marker, was established, thus defining a chromosomal locus for sulr-c. DNA isolated from sulr-c cells transforms two mutant recipient strains at the same low efficiency as it does a wild-type recipient, although the mutant property of these strains makes them capable of integrating classical "low-efficiency" donor markers equally as efficiently as "high efficiency" markers. Hence sulr-c must have a different basis for its low efficiency than do classical low efficiency point mutations. We suggest that the DNA in the region of the sulr-c mutation has a structural abnormality which leads both to its frequent segregation during growth and its difficulty in efficiently mediating genetic transformation.

scholarly journals Osteopontin Deficiency Induces Parathyroid Hormone Enhancement of Cortical Bone Formation

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2132-2140 ◽  
Author(s):  
Keiichiro Kitahara ◽  
Muneaki Ishijima ◽  
Susan R. Rittling ◽  
Kunikazu Tsuji ◽  
Hisashi Kurosawa ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Formation ◽  
Bone Mass ◽  
Cortical Bone ◽  
Cancellous Bone ◽  
Wild Type ◽  
Mineral Density ◽  
Cortical Bone Mass ◽  
Intermittent Pth

Intermittent PTH treatment increases cancellous bone mass in osteoporosis patients; however, it reveals diverse effects on cortical bone mass. Underlying molecular mechanisms for anabolic PTH actions are largely unknown. Because PTH regulates expression of osteopontin (OPN) in osteoblasts, OPN could be one of the targets of PTH in bone. Therefore, we examined the role of OPN in the PTH actions in bone. Intermittent PTH treatment neither altered whole long-bone bone mineral density nor changed cortical bone mass in wild-type 129 mice, although it enhanced cancellous bone volume as reported previously. In contrast, OPN deficiency induced PTH enhancement of whole-bone bone mineral density as well as cortical bone mass. Strikingly, although PTH suppressed periosteal bone formation rate (BFR) and mineral apposition rate (MAR) in cortical bone in wild type, OPN deficiency induced PTH activation of periosteal BFR and MAR. In cancellous bone, OPN deficiency further enhanced PTH increase in BFR and MAR. Analysis on the cellular bases for these phenomena indicated that OPN deficiency augmented PTH enhancement in the increase in mineralized nodule formation in vitro. OPN deficiency did not alter the levels of PTH enhancement of the excretion of deoxypyridinoline in urine, the osteoclast number in vivo, and tartrate-resistant acid phosphatase-positive cell development in vitro. These observations indicated that OPN deficiency specifically induces PTH activation of periosteal bone formation in the cortical bone envelope.

scholarly journals exrB: amalB-linked gene inEscherichia coliB involved in sensitivity to radiation and filament formation

1974 ◽  
Vol 23 (2) ◽  
pp. 175-184 ◽  
Author(s):  
Joseph Greenberg ◽  
Leonard J. Berends ◽  
John Donch ◽  
Michael H. L. Green
Keyword(s):  
Escherichia Coli ◽  
Normal Growth ◽  
Filament Formation ◽  
Wild Type ◽  
Sensitive Mutant ◽  
Γ Radiation ◽  
Linked Gene ◽  
Derivatives Of

SUMMARYPAM 26, a radiation-sensitive mutant ofEscherichia colistrain B, is described. Its properties are attributable to a mutation in a gene,exrB, which is cotransducible withmalB. It differs fromuvrA(alsomalB-linked) derivatives of strain B in being sensitive to 1-methyl-3-nitro-1-nitroso-guanidine and γ-radiation, and in being able to reactivate UV-irradiated phage T3. It differs fromexrA(alsomalB-linked) derivatives of strain B in forming filaments during the course of normal growth as well as after irradiation. WhenexrBwas transduced into a K12 (lon+) strain, filaments did not form spontaneously. Three-point transductions established the order of markers asmet A malB exrB. Based on an analysis of the frequency of wild-type recombinants in a reciprocal transduction betweenexrAandexrBstrains, it was inferred that they are not isogenic and that the order of markers ismalB exrA exrB.

Investigation on the origin of the definitive endoderm in the rat embryo

Development ◽  
1974 ◽  
Vol 32 (2) ◽  
pp. 445-459
Author(s):  
B. Levak-Švajger ◽  
A. Švajger
Keyword(s):  
Primitive Streak ◽  
Definitive Endoderm ◽  
Rat Embryo ◽  
Chick Blastoderm ◽  
Germ Layers ◽  
Kidney Capsule ◽  
Rat Embryos ◽  
Endodermal Cells ◽  
Derivatives Of

Single germ layers (or combinations of two of them) were isolated from the primitive streak and the head-fold stage rat embryos and grown for 15 days under the kidney capsule of syngeneic adult animals. The resulting teratomas were examined histologically for the presence of mature tissues, with special emphasis on derivatives of the primitive gut. Ectoderm isolated together with the initial mesodermal wings at the primitive streak stage gave rise to tissue derivatives of all three definitive germ layers. Derivatives of the primitive gut were regularly present in these grafts. At the head-fold stage, isolated ectoderm (including the region of the primitive streak) differentiated into ectodermal and mesodermal derivatives only. Endoderm isolated at the primitive streak stage did not develop when grafted and was always completely resorbed. At the head-fold stage, however, definitive endoderm differentiated into derivatives of the primitive gut if grafted together with adjacent mesoderm. These findings indirectly suggest the migration of prospective endodermal cells from the primitive ectoderm, and therefore a general analogy with the course of events during gastrulation in the chick blastoderm.

scholarly journals Altering the Ratio of Phenazines in Pseudomonas chlororaphis (aureofaciens) Strain 30-84: Effects on Biofilm Formation and Pathogen Inhibition

2008 ◽  
Vol 190 (8) ◽  
pp. 2759-2766 ◽  
Author(s):  
V. S. R. K. Maddula ◽  
E. A. Pierson ◽  
L. S. Pierson
Keyword(s):  
Fungal Pathogen ◽  
Biofilm Formation ◽  
Flow Cell ◽  
Gaeumannomyces Graminis ◽  
Pseudomonas Chlororaphis ◽  
Wild Type ◽  
Initial Attachment ◽  
Pathogen Inhibition ◽  
Biofilm Development ◽  
Derivatives Of

ABSTRACT Pseudomonas chlororaphis strain 30-84 is a plant-beneficial bacterium that is able to control take-all disease of wheat caused by the fungal pathogen Gaeumannomyces graminis var. tritici. The production of phenazines (PZs) by strain 30-84 is the primary mechanism of pathogen inhibition and contributes to the persistence of strain 30-84 in the rhizosphere. PZ production is regulated in part by the PhzR/PhzI quorum-sensing (QS) system. Previous flow cell analyses demonstrated that QS and PZs are involved in biofilm formation in P. chlororaphis (V. S. R. K. Maddula, Z. Zhang, E. A. Pierson, and L. S. Pierson III, Microb. Ecol. 52:289-301, 2006). P. chlororaphis produces mainly two PZs, phenazine-1-carboxylic acid (PCA) and 2-hydroxy-PCA (2-OH-PCA). In the present study, we examined the effect of altering the ratio of PZs produced by P. chlororaphis on biofilm formation and pathogen inhibition. As part of this study, we generated derivatives of strain 30-84 that produced only PCA or overproduced 2-OH-PCA. Using flow cell assays, we found that these PZ-altered derivatives of strain 30-84 differed from the wild type in initial attachment, mature biofilm architecture, and dispersal from biofilms. For example, increased 2-OH-PCA production promoted initial attachment and altered the three-dimensional structure of the mature biofilm relative to the wild type. Additionally, both alterations promoted thicker biofilm development and lowered dispersal rates compared to the wild type. The PZ-altered derivatives of strain 30-84 also differed in their ability to inhibit the fungal pathogen G. graminis var. tritici. Loss of 2-OH-PCA resulted in a significant reduction in the inhibition of G. graminis var. tritici. Our findings suggest that alterations in the ratios of antibiotic secondary metabolites synthesized by an organism may have complex and wide-ranging effects on its biology.

Occurrence of embryotoxicity in mouse embryos following in utero exposure to 2′-deoxycoformycin (pentostatin)

Teratology ◽  
1993 ◽  
Vol 47 (1) ◽  
pp. 17-27 ◽  
Author(s):  
Mark J. Airhart ◽  
Charles M. Robbins ◽  
Thomas B. Knudsen ◽  
Joyce K. Church ◽  
Richard G. Skalko
Keyword(s):  
In Utero ◽  
Mouse Embryos ◽  
In Utero Exposure

scholarly journals Differential ability of a T-antigen transport-defective mutant of simian virus 40 to transform primary and established rodent cells.

1985 ◽  
Vol 5 (5) ◽  
pp. 1043-1050 ◽  
Author(s):  
R E Lanford ◽  
C Wong ◽  
J S Butel
Keyword(s):  
Cell Lines ◽  
Mouse Embryo ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Wild Type ◽  
Mouse Embryo Fibroblasts ◽  
Established Cell Lines ◽  
Established Cell ◽  
Embryo Fibroblasts

The transforming potential and oncogenicity of a simian virus 40 (SV40) mutant affecting T-antigen (T-ag), SV40(cT)-3, was examined in an effort to dissect T-ag functions in transformation. SV40(cT)-3 has a point mutation at nucleotide 4434 that abolishes the transport of T-ag to the nucleus but does not affect its association with the cell surface. Transfection-transformation assays were performed with primary cells and established cell lines of mouse and rat origin. The efficiency of transformation for established cell lines by SV40(cT)-3 was comparable to that of wild-type SV40, indicating that transformation of established cell lines can occur in the absence of detectable amounts of nuclear T-ag. Transformation of primary mouse embryo fibroblasts by SV40(cT)-3 was markedly influenced by culture conditions; the relative transforming frequency was dramatically reduced in assays involving focus formation in low serum concentrations or anchorage-independent growth. Immunofluorescence tests revealed that the transformed mouse embryo fibroblasts partially transport the mutant cT-ag to the cell nucleus. Transformed cell lines induced by SV40(cT)-3 did not differ in growth properties from wild-type transformants. SV40(cT)-3 was completely defective for the transformation of primary baby rat kidney cells, a primary cell type unable to transport the mutant T-ag to the nucleus. The intracellular localization of cellular protein p53 was found to mimic T-ag distribution in all the transformants analyzed. The mutant virus was weakly oncogenic in vivo: the induction of tumors in newborn hamsters by SV40(cT)-3 was reduced in incidence and delayed in appearance in comparison to wild-type SV40. These observations suggest that cellular transformation is regulated by both nuclear and surface-associated forms of SV40 T-ag.

Studies of t6/t6 mouse embryos

Development ◽  
1975 ◽  
Vol 33 (3) ◽  
pp. 697-713
Author(s):  
Mary Nadijcka ◽  
Nina Hillman
Keyword(s):  
Lipid Droplets ◽  
Mouse Embryos ◽  
Wild Type ◽  
Electron Microscopic ◽  
Homozygous Mouse ◽  
Cytoplasmic Lipid Droplets

The phenocritical period of the t6/t6 genome extends from the late blastocyst substages through the elongated egg-cylinder stage, whereas the lethal period begins at the short egg-cylinder-stage and extends through the elongated egg-cylinder stage. Most of the homozygous mouse embryos die during the short egg-cylinder stage. The viable egg-cylinder-staged t6/t6 embryos can be distinguished from their phenotypically wild-type litter-mates at both the light and electron microscopic levels. The distinguishing characteristics of these embryos are aberrantly arranged entodermal cells, excessive cytoplasmic lipid and crystal-containing mitochondria. These same features are also characteristic of those mutant embryos which are developmentally arrested at both the short and elongated egg-cylinder stages. Over 50% of the t6/t6 embryos can be identified as early as the late blastocyst substages by the presence of large, electron-dense cytoplasmic lipid droplets.

Sign in / Sign up

Export Citation Format

Share Document