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.

Vitrification of porcine early cleavage stage embryos and oocytes after removal of cytoplasmic lipid droplets

1996 ◽  
Vol 45 (1) ◽  
pp. 180 ◽  
Author(s):  
H. Nagashima ◽  
M. Kuwayama ◽  
C.G. Grupen ◽  
R.J. Ashman ◽  
M.B. Nottle
Keyword(s):  
Lipid Droplets ◽  
Cleavage Stage ◽  
Early Cleavage ◽  
Cytoplasmic Lipid Droplets

scholarly journals STUDIES ON MICROPEROXISOMES II. A CYTOCHEMICAL METHOD FOR LIGHT AND ELECTRON MICROSCOPY

1972 ◽  
Vol 20 (12) ◽  
pp. 1006-1023 ◽  
Author(s):  
ALEX B. NOVIKOFF ◽  
PHYLLIS M. NOVIKOFF ◽  
CLEVELAND DAVIS ◽  
NELSON QUINTANA
Keyword(s):  
Endoplasmic Reticulum ◽  
Guinea Pig ◽  
Lipid Droplets ◽  
Smooth Endoplasmic Reticulum ◽  
Light And Electron Microscopy ◽  
Distal Tubule ◽  
Striking Difference ◽  
High Concentration ◽  
Electron Microscopic ◽  
Pig Kidney

A modification of the Novikoff-Goldfischer alkaline 3,3'-diaminobenzidine medium for visualizing peroxisomes is described. It makes possible light microscopic as well as electron microscopic studies of a recently described class of peroxisomes, the microperoxisomes. Potassium cyanide (5 x 10–3 M) is included in the medium to inhibit mitochondrial staining, the pH is 9.7 and there is a high concentration of H2O2 (0.05%). Two cell types have been chosen to illustrate the advantages of the new procedure for demonstrating the microperoxisomes: the absorptive cells in the human jejunum and the distal tubule cells in the guinea pig kidney. Suggestive relations of microperoxisomes and lipid are described in the human jejunum. The microperoxisomes are strategically located between smooth endoplasmic reticulum that radiates toward the organelles and contains lipid droplets and "central domains" of highly specialized endoplasmic reticulum which do not show the lipid droplets. The microperoxisomes are also present at the periphery of large lipid-like drops. In the guinea pig kidney tubule there is a striking difference between the thick limb of Henle and distal tubule. The distal tubule has a population of cells with large numbers of microperoxisomes readily visible by light microscopy; these cells are not present in the thick limb of Henle. Other differences between the two are also described.

scholarly journals Roles of rpoN, fliA,and flgR in Expression of Flagella inCampylobacter jejuni

2001 ◽  
Vol 183 (9) ◽  
pp. 2937-2942 ◽  
Author(s):  
Aparna Jagannathan ◽  
Chrystala Constantinidou ◽  
Charles W. Penn
Keyword(s):  
Campylobacter Jejuni ◽  
Genome Sequence ◽  
Sigma Factor ◽  
Transcriptional Activator ◽  
Alternative Sigma Factor ◽  
Wild Type ◽  
Electron Microscopic ◽  
Global Regulation ◽  
Mutant Strains ◽  
Microscopic Studies

ABSTRACT Three potential regulators of flagellar expression present in the genome sequence of Campylobacter jejuni NCTC 11168, the genes rpoN, flgR, andfliA, which encode the alternative sigma factor ς54, the ς54-associated transcriptional activator FlgR, and the flagellar sigma factor ς28, respectively, were investigated for their role in global regulation of flagellar expression. The three genes were insertionally inactivated inC. jejuni strains NCTC 11168 and NCTC 11828. Electron microscopic studies of the wild-type and mutant strains showed that therpoN and flgR mutants were nonflagellate and that the fliA mutant had truncated flagella. Immunoblotting experiments with the three mutants confirmed the roles of rpoN, flgR, and fliA in the expression of flagellin.

Effect of various inhibitors on sporulation of Bacillus subtilis crs mutants

1984 ◽  
Vol 30 (11) ◽  
pp. 1337-1343 ◽  
Author(s):  
I. Takahashi ◽  
Dongxu Sun
Keyword(s):  
Bacillus Subtilis ◽  
Microscopic Examination ◽  
Electron Microscopic Examination ◽  
Aliphatic Alcohols ◽  
Wild Type ◽  
Electron Microscopic

The effect of aliphatic alcohols, cerulenin, and NaCl on sporulation of various catabolite-resistant (crs) mutants of Bacillus subtilis was studied. Mutants carrying crsA or crsF mutations were able to sporulate in the presence of these agents. Other crs mutants were resistant to at least one of the inhibitors. Electron microscopic examination revealed that cerulenin blocks sporulation at stage 0 in wild-type cells, suggesting that early sporulation functions are affected by this antibiotic. The results obtained so far suggest that the functions altered in the crs mutants may be related to the membrane.

scholarly journals Recent Progress in Cryopreservation of Bovine Oocytes

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
In-Sul Hwang ◽  
Shinichi Hochi
Keyword(s):  
Lipid Droplets ◽  
Coiled Coil ◽  
High Sensitivity ◽  
Short Term ◽  
Rock Inhibitor ◽  
Developmental Potential ◽  
Domestic Species ◽  
Cytoplasmic Lipid Droplets ◽  
Recovery Culture ◽  
Bovine Oocytes

Principle of oocyte cryoinjury is first overviewed and then research history of cryopreservation using bovine oocytes is summarized for the last two decades with a few special references to recent progresses. Various types of cryodevices have been developed to accelerate the cooling rate and applied to the oocytes from large domestic species enriched with cytoplasmic lipid droplets. Two recent approaches include the qualitative improvement of IVM oocytes prior to the vitrification and the short-term recovery culture of vitrified-warmed oocytes prior to the subsequent IVF. Supplementation of L-carnitine to IVM medium of bovine oocytes has been reported to reduce the amount of cytoplasmic lipid droplets and improve the cryotolerance of the oocytes, but it is still controversial whether the positive effect of L-carnitine is reproducible. Incidence of multiple aster formation, a possible cause for low developmental potential of vitrified-warmed bovine oocytes, was inhibited by a short-term culture of the postwarm oocytes in the presence of Rho-associated coiled-coil kinase (ROCK) inhibitor. Use of an antioxidantα-tocopherol, instead of the ROCK inhibitor, also supported the revivability of the postwarm bovine oocytes. Further improvements of the vitrification procedure, combined with pre- and postvitrification chemical treatment, would overcome the high sensitivity of bovine oocytes to cryopreservation.

scholarly journals Phosphatidylcholine transfer protein/StarD2 promotes microvesicular steatosis and liver injury in murine experimental steatohepatitis

2017 ◽  
Vol 313 (1) ◽  
pp. G50-G61 ◽  
Author(s):  
Hayley T. Nicholls ◽  
Jason L. Hornick ◽  
David E. Cohen
Keyword(s):  
Liver Injury ◽  
Lipid Droplets ◽  
Plasma Concentrations ◽  
Fibroblast Growth Factor 21 ◽  
Wild Type ◽  
Hepatocellular Injury ◽  
Pathogenic Role ◽  
Deficient Diet ◽  
Transfer Protein ◽  
Phosphatidylcholine Transfer Protein

Mice fed a methionine- and choline-deficient (MCD) diet develop steatohepatitis that recapitulates key features of nonalcoholic steatohepatitis (NASH) in humans. Phosphatidylcholine is the most abundant phospholipid in the surfactant monolayer that coats and stabilizes lipid droplets within cells, and choline is required for its major biosynthetic pathway. Phosphatidylcholine-transfer protein (PC-TP), which exchanges phosphatidylcholines among membranes, is enriched in hepatocytes. PC-TP also regulates fatty acid metabolism through interactions with thioesterase superfamily member 2. We investigated the contribution of PC-TP to steatohepatitis induced by the MCD diet. Pctp−/− and wild-type control mice were fed the MCD diet for 5 wk and were then euthanized for histopathologic and biochemical analyses, as well as determinations of mRNA and protein expression. Whereas all mice developed steatohepatitis, plasma alanine aminotransferase and aspartate aminotransferase activities were only elevated in wild-type mice, indicating that Pctp−/− mice were protected from MCD diet-induced hepatocellular injury. Reduced hepatotoxicity due to the MCD diet in the absence of PC-TP expression was further evidenced by decreased activation of c-Jun and reduced plasma concentrations of fibroblast growth factor 21. Despite similar total hepatic concentrations of phosphatidylcholines and other lipids, the relative abundance of microvesicular lipid droplets within hepatocytes was reduced in Pctp−/− mice. Considering that the formation of larger lipid droplets may serve to protect against lipotoxicity in NASH, our findings suggest a pathogenic role for PC-TP that could be targeted in the management of this condition. NEW & NOTEWORTHY Phosphatidylcholine-transfer protein (PC-TP) is a highly specific phosphatidylcholine-binding protein that we previously showed to regulate hepatocellular nutrient metabolism through its interacting partner thioesterase superfamily member 2 (Them2). This study identifies a pathogenic role for PC-TP, independent of Them2, in the methionine- and choline-deficient diet model of experimental steatohepatitis. Our current observations suggest that PC-TP promotes liver injury by mediating the intermembrane transfer of phosphatidylcholines, thus stabilizing more pathogenic microvesicular lipid droplets.

Abstract 15445: The Sirtuin SIRT3 Blocks Doxorubicin-induced Cardiac Hypertrophic Response of Mice

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Vinodkumar Pillai ◽  
Sadhana Samant ◽  
Nagalingam Sundaresan ◽  
Gene Kim ◽  
Mahesh P Gupta
Keyword(s):  
Negative Regulator ◽  
Neonatal Rat ◽  
Whole Body ◽  
Wild Type ◽  
Electron Microscopic ◽  
Specific Expression ◽  
Rat Cardiomyocytes ◽  
Fluorescent Intensity ◽  
Hypertrophic Response

Background and objective: Doxorubicin is a chemotherapeutic drug widely used to treat variety of cancers. One of the serious side effects of doxorubicin is its toxicity to the heart. Previously, we have shown that overexpression of SIRT3 blocks the hypertrophic response of the heart to agonist treatments. This study was undertaken to investigate whether SIRT3 can also attenuate the doxorubicin-induced cardiac hypertrophic response in mice. Methods and results: Neonatal rat cardiomyocytes overexpressed with SIRT3 and treated with doxorubicin (10μM) showed 28% reduced mean fluorescent intensity for CM-H 2 DCFDA dye, compared to mock infected control cells treated with doxorubicin, thus suggesting that SIRT3 was capable of blocking doxorubicin-induced ROS synthesis in cardiomyocytes. To examine the cardioprotective effects of SIRT3 in doxorubicin-induced cardiotoxicity in vivo ; we used a cumulative dose of 15mg/kg of doxorubicin for two different time points. One group of mice was treated intraperitoneally with 5mg/kg doxorubicin or an equal volume of saline every two weeks for a total of three doses. Transgenic mice having cardiac specific expression of SIRT3 (SIRT3-Tg) showed 33% reduced HW/BW ratio compared to control mice. Echocardiographic evaluation of hearts showed significantly reduced fractional shortening in control mice, compared to SIRT3-Tg mice (24.6 vs 34.7 %, P<0.05). SIRT3-Tg mice also showed significantly reduced fetal gene expression for ANF, βMHC and collagen-1 as determined by RT-PCR. Masson’s trichrome staining showed significantly reduced fibrosis in doxorubicin treated SIRT3-Tg mice compared to its control. Furthermore, electron microscopic analysis showed preserved mitochondrial and sarcomeres structures in doxorubicin treated SIRT3-Tg hearts, whereas in wild-type hearts these structures were highly disorganized. Second group of mice that received 15mg/kg dose for two weeks also showed similar results. Contrary to this, whole body SIRT3 knockout mice showed exacerbated cardiac hypertrophic response compared to wild-type mice in response to doxorubicin treatment. Conclusion: These results demonstrated that SIRT3 is an endogenous negative regulator of doxorubicin-induced cardiac hypertrophic response.

scholarly journals The molecular chaperone Hsp90α deficiency causes retinal degeneration by disrupting Golgi organization and vesicle transportation in photoreceptors

2019 ◽  
Vol 12 (3) ◽  
pp. 216-229 ◽  
Author(s):  
Yuan Wu ◽  
Xiudan Zheng ◽  
Yubo Ding ◽  
Min Zhou ◽  
Zhuang Wei ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Molecular Chaperone ◽  
Outer Segment ◽  
Microscopic Analysis ◽  
Heat Shock Protein 90 ◽  
Hsp90 Inhibitor ◽  
Wild Type ◽  
Electron Microscopic ◽  
Golgi Organization ◽  
Deficient Mice

Abstract Heat shock protein 90 (Hsp90) is an abundant molecular chaperone with two isoforms, Hsp90α and Hsp90β. Hsp90β deficiency causes embryonic lethality, whereas Hsp90α deficiency causes few abnormities except male sterility. In this paper, we reported that Hsp90α was exclusively expressed in the retina, testis, and brain. Its deficiency caused retinitis pigmentosa (RP), a disease leading to blindness. In Hsp90α-deficient mice, the retina was deteriorated and the outer segment of photoreceptor was deformed. Immunofluorescence staining and electron microscopic analysis revealed disintegrated Golgi and aberrant intersegmental vesicle transportation in Hsp90α-deficient photoreceptors. Proteomic analysis identified microtubule-associated protein 1B (MAP1B) as an Hsp90α-associated protein in photoreceptors. Hspα deficiency increased degradation of MAP1B by inducing its ubiquitination, causing α-tubulin deacetylation and microtubule destabilization. Furthermore, the treatment of wild-type mice with 17-DMAG, an Hsp90 inhibitor of geldanamycin derivative, induced the same retinal degeneration as Hsp90α deficiency. Taken together, the microtubule destabilization could be the underlying reason for Hsp90α deficiency-induced RP.

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