Mesenchymal cells engulf and clear apoptotic footplate cells in macrophageless PU.1 null mouse embryos

Development ◽  
2000 ◽  
Vol 127 (24) ◽  
pp. 5245-5252 ◽  
Author(s):  
W. Wood ◽  
M. Turmaine ◽  
R. Weber ◽  
V. Camp ◽  
R.A. Maki ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Body Shape ◽  
Mouse Embryos ◽  
Null Mouse ◽  
Wild Type ◽  
Wild Type Embryo ◽  
Cell Numbers ◽  
Embryonic Tissues ◽  
In The Wild ◽  
Clearance Process

Apoptosis is one of the key tools used by an embryo to regulate cell numbers and sculpt body shape. Although massive numbers of cells die during development, they are so rapidly phagocytosed that very few corpses are ever seen in most embryonic tissues. In this paper, we focus on the catastrophic cell death that occurs as the developing footplate is remodelled to transform webbed regions into free interdigital spaces. In the wild-type embryo, these dead cells are rapidly engulfed and cleared by macrophages. We show that in a macrophageless mouse embryo, null for the haemopoetic-lineage-specific transcription factor, PU.1, the task of phagocytosis is taken over by ‘stand-in’ mesenchymal neighbours in a clear example of cell redundancy. However, it takes three times as many of these mesenchymal phagocytes to complete the task and, at each stage of the clearance process - in the recognition of apoptotic debris, its engulfment and finally its digestion - they appear to be less efficient than macrophages. A molecular explanation for this may be that several of the engulfment genes expressed by macrophages, including the ABC1 transporter (believed to be part of the phagocytic machinery conserved from Caenorhabditis elegans to mouse), are not upregulated by these ‘stand-in’ phagocytes.

scholarly journals Predisposition to Arrhythmia and Autonomic Dysfunction in Nhlh1-Deficient Mice

2002 ◽  
Vol 22 (14) ◽  
pp. 4977-4983 ◽  
Author(s):  
Tiziana Cogliati ◽  
Deborah J. Good ◽  
Mark Haigney ◽  
Petra Delgado-Romero ◽  
Michael A. Eckhaus ◽  
...  
Keyword(s):  
Nervous System ◽  
Transcription Factor ◽  
Wild Type Mouse ◽  
Heart Rhythm ◽  
Mutant Mice ◽  
Null Mouse ◽  
Unexpected Death ◽  
Experimental Conditions ◽  
Helix Loop Helix ◽  
In The Wild

ABSTRACT Nhlh1 is a basic helix-loop-helix transcription factor whose expression is restricted to the nervous system and which may play a role in neuronal differentiation. To directly study Nhlh1 function, we generated null mice. Homozygous mutant mice were predisposed to premature, adult-onset, unexpected death. Electrocardiograms revealed decreased total heart rate variability, stress-induced arrhythmia, and impaired baroreceptor sensitivity. This predisposition to arrhythmia is a likely cause of the observed death in the mutant mice. Heterozygosity for the closely related transcription factor Nhlh2 increased the severity of the Nhlh1-null phenotype. No signs of primary cardiac structural or conduction abnormalities could be detected upon necropsy of the null mice. The pattern of altered heart rhythm observed in basal and experimental conditions (stress and pharmacologically induced) suggests that a deficient parasympathetic tone may contribute to the arrhythmia in the Nhlh1-null mouse. The expression of Nhlh1 in the developing brain stem and in the vagal nuclei in the wild-type mouse further supports this hypothesis. The Nhlh1 mutant mouse may thus provide a model to investigate the contribution of the autonomic nervous system to arrhythmogenesis.

The pattern of proliferation of the neuroblasts in the wild-type embryo of Drosophila melanogaster

1987 ◽  
Vol 196 (8) ◽  
pp. 473-485 ◽  
Author(s):  
Volker Hartenstein ◽  
Eberhard Rudloff ◽  
Jose A. Campos -Ortega
Keyword(s):  
Drosophila Melanogaster ◽  
Wild Type ◽  
Wild Type Embryo ◽  
In The Wild

A white mutant of Malay apple fruit (Syzygium malaccense) lacks transcript expression and activity for the last enzyme of anthocyanin synthesis, and the normal expression of a MYB transcription factor

2011 ◽  
Vol 38 (1) ◽  
pp. 75 ◽  
Author(s):  
Panumas Kotepong ◽  
Saichol Ketsa ◽  
Wouter G. van Doorn
Keyword(s):  
Transcription Factor ◽  
Myb Transcription Factor ◽  
Anthocyanin Synthesis ◽  
Wild Type ◽  
Fruit Maturation ◽  
Total Anthocyanin ◽  
White Skin ◽  
Fruit Skin ◽  
In The Wild ◽  
White Mutant

The fruit skin of the mature Malay apple (Syzygium malaccense (L.) Merr. & L.M. Perry) is initially glossy red, then changes to purple. A mutant having mature fruits with white skin has been identified. The skin of wild-type fruit contained five glucose-based anthocyanins (cyanidin-3-O-glucoside, pelargonidin-3-O-glucoside, peonidin-3-O-glucoside, cyanidin-3,5-O-diglucoside and peonidin-3,5-O-diglucoside). Cyanidin-3-O-glucoside accounted for a large proportion of the total anthocyanin content. The accumulation cyanidin-3-O-glucoside during fruit maturation was correlated with increased activities of phenylalanine ammonia lyase (PAL) and UDPglucose : flavonoid 3-O-glucosyltransferase (UF3GlucT, F3GT). In the wild-type fruit skin, transcripts of seven genes that encode enzymes in the anthocyanin biosynthetic pathway were detected. No anthocyanins were found in the white mutant fruit skin. The skin of the white mutant fruit contained transcripts of all seven genes identified, except F3GT. It also showed no F3GT activity. The data indicate that the lack of anthocyanins in the mutant is due to lack of F3GT expression. In addition, the transcript of a MYB transcription factor, highly homologous to three Arabidopsis MYBs involved in anthocyanin synthesis, was virtually absent in the mutant but very high in the wild-type fruit. It is suggested that the lack of MYB expression is part of the cause of the lack of F3GT expression and anthocyanin synthesis during fruit maturation.

Accentuated response to phenylhydrazine and erythropoietin in mice genetically impaired for their GATA-1 expression (GATA-1low mice)

Blood ◽  
2001 ◽  
Vol 97 (10) ◽  
pp. 3040-3050 ◽  
Author(s):  
Alessandro Maria Vannucchi ◽  
Lucia Bianchi ◽  
Cristina Cellai ◽  
Francesco Paoletti ◽  
Valentina Carrai ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Precursor Cells ◽  
Cell Populations ◽  
Wild Type ◽  
Erythroid Progenitor ◽  
Cell Numbers ◽  
Erythroid Progenitor Cells ◽  
Colony Forming Units ◽  
In The Wild

Abstract The response of mice genetically unable to up-regulate GATA-1 expression (GATA-1low mice) to acute (phenylhydrazine [PHZ]–induced anemia) and chronic (in vivo treatment for 5 days with 10 U erythropoietin [EPO] per mouse) erythroid stimuli was investigated. Adult GATA-1low mice are profoundly thrombocytopenic (platelet counts [× 109/L] 82.0 ± 28.0 vs 840 ± 170.0 of their control littermates, P < .001) but have a normal hematocrit (Hct) (approximately .47 proportion of 1.0 [47%]). The spleens of these mutants are 2.5-fold larger than normal and contain 5-fold more megakaryocytic (4A5+), erythroid (TER-119+), and bipotent (erythroid/megakaryocytic, TER-119+/4A5+) precursor cells. Both the marrow and the spleen of these animals contain higher frequencies of burst-forming units–erythroid (BFU-E)– and colony-forming units–erythroid (CFU-E)–derived colonies (2-fold and 6-fold, respectively) than their normal littermates. The GATA-1low mice recover 2 days faster from the PHZ-induced anemia than their normal littermates (P < .01). In response to EPO, the Hct of the GATA-1low mice raised to .68 proportion of 1.0 (68%) vs the .55 proportion of 1.0 (55%) reached by the controls (P < .01). Both the GATA-1low and the normal mice respond to PHZ and EPO with similar (2- to 3-fold) increases in size and cellularity of the spleen (increases are limited mostly to cells, both progenitor and precursor, of the erythroid lineage). However, in spite of the similar relative cellular increases, the increases of all these cell populations are significantly higher, in absolute cell numbers, in the mutant than in the wild-type mice. In conclusion, the GATA-1low mutation increases the magnitude of the response to erythroid stimuli as a consequence of the expansion of the erythroid progenitor cells in their spleen.

scholarly journals Microarray analysis of Arabidopsis WRKY33 mutants in response to the necrotrophic fungus Botrytis cinerea

2018 ◽  
Author(s):  
Synan AbuQamar ◽  
Khaled Moustafa
Keyword(s):  
Transcription Factor ◽  
Botrytis Cinerea ◽  
Defense Responses ◽  
Plant Responses ◽  
Wild Type Plant ◽  
The Novel ◽  
Wild Type ◽  
Genes Encoding ◽  
In The Wild ◽  
Molecular Components

The WRKY33 transcription factor was reported for resistance to the necrotrophic fungus Botrytis cinerea. Using microarray-based analysis, we compared Arabidopsis WRKY33 overexpressing lines and wrky33 mutant that showed altered susceptibility to B. cinerea with their corresponding wild-type plants. In the wild-type, about 1660 genes (7% of the transcriptome) were induced and 1054 genes (5% of the transcriptome) were repressed at least twofold at early stages of inoculation with B. cinerea, confirming previous data of the contribution of these genes in B. cinerea resistance. In Arabidopsis wild-type plant infected with B. cinerea, the expressions of the differentially expressed genes encoding for proteins and metabolites involved in pathogen defense and non-defense responses, seem to be dependent on a functional WRKY33 gene. The expression profile of 12-oxo-phytodienoic acid- and phytoprostane A1-treated Arabidopsis plants in response to B. cinerea revealed that cyclopentenones can also modulate WRKY33 regulation upon inoculation with B. cinerea. These results support the role of electrophilic oxylipins in mediating plant responses to B. cinerea infection through the TGA transcription factor. Future directions toward the identification of the molecular components in cyclopentenone signaling will elucidate the novel oxylipin signal transduction pathways in plant defense.

scholarly journals Transketolase Haploinsufficiency Reduces Adipose Tissue and Female Fertility in Mice

2002 ◽  
Vol 22 (17) ◽  
pp. 6142-6147 ◽  
Author(s):  
Zheng-Ping Xu ◽  
Eric F. Wawrousek ◽  
Joram Piatigorsky
Keyword(s):  
Adipose Tissue ◽  
Metabolic Pathways ◽  
Well Being ◽  
Threshold Level ◽  
Mouse Embryos ◽  
Null Mouse ◽  
Wild Type ◽  
Small Female ◽  
Female Ratio ◽  
Male Female Ratio

ABSTRACT Transketolase (TKT) is a ubiquitous enzyme used in multiple metabolic pathways. We show here by gene targeting that TKT-null mouse embryos are not viable and that disruption of one TKT allele can cause growth retardation (≈35%) and preferential reduction of adipose tissue (≈77%). Other TKT+/− tissues had moderate (≈33%; liver, gonads) or relatively little (≈7 to 18%; eye, kidney, heart, brain) reductions in mass. These mice expressed a normal level of growth hormone and reduced leptin levels. No phenotype was observed in the TKT+/− cornea, where TKT is especially abundant in wild-type mice. The small female TKT+/− mice mated infrequently and had few progeny (with a male/female ratio of 1.4:1) when pregnant. Thus, TKT in normal mice appears to be carefully balanced at a threshold level for well-being. Our data suggest that TKT deficiency may have clinical significance in humans and raise the possibility that obesity may be treated by partial inhibition of TKT in adipose tissue.

scholarly journals The ATF/CREB Transcription Factor Atf1 Is Essential for Full Virulence, Deoxynivalenol Production, and Stress Tolerance in the Cereal Pathogen Fusarium graminearum

2013 ◽  
Vol 26 (12) ◽  
pp. 1378-1394 ◽  
Author(s):  
Thuat Van Nguyen ◽  
Cathrin Kröger ◽  
Jakob Bönnighausen ◽  
Wilhelm Schäfer ◽  
Jörg Bormann
Keyword(s):  
Transcription Factor ◽  
Osmotic Stress ◽  
Fusarium Graminearum ◽  
Brachypodium Distachyon ◽  
Constitutive Expression ◽  
Mitogen Activated Protein Kinase ◽  
Wild Type ◽  
Mitogen Activated Protein ◽  
In The Wild

Fusarium graminearum is a necrotrophic plant pathogen of cereals that produces mycotoxins such as deoxynivalenol (DON) and zearalenone (ZEA) in grains. The stress-activated mitogen-activated protein kinase FgOS-2 is a central regulator in F. graminearum and controls, among others, virulence and DON and ZEA production. Here, we characterized the ATF/CREB-activating transcription factor FgAtf1, a regulator that functions downstream of FgOS-2. We created deletion and overexpression mutants of Fgatf1, the latter being also in an FgOS-2 deletion mutant. FgAtf1 localizes to the nucleus and appears to interact with FgOS-2 under osmotic stress conditions. Deletion mutants in Fgatf1 (ΔFgatf1) are more sensitive to osmotic stress and less sensitive to oxidative stress compared with the wild type. Furthermore, sexual reproduction is delayed. ΔFgatf1 strains produced higher amounts of DON under in vitro induction conditions than that of the wild type. However, during wheat infection, DON production by ΔFgatf1 is strongly reduced. The ΔFgatf1 strains displayed strongly reduced virulence to wheat and maize. Interestingly, constitutive expression of Fgatf1 in the wild type led to hypervirulence on wheat, maize, and Brachypodium distachyon. Moreover, constitutive expression of Fgatf1 in the ΔFgOS-2 mutant background almost complements ΔFgOS-2-phenotypes. These data suggest that FgAtf1 may be the most important transcription factor regulated by FgOS-2.

scholarly journals Purine Biosynthesis, Riboflavin Production, and Trophic-Phase Span Are Controlled by a Myb-Related Transcription Factor in the Fungus Ashbya gossypii

2006 ◽  
Vol 72 (7) ◽  
pp. 5052-5060 ◽  
Author(s):  
Laura Mateos ◽  
Alberto Jiménez ◽  
José L. Revuelta ◽  
María A. Santos
Keyword(s):  
Transcription Factor ◽  
Dna Analysis ◽  
Fluorescent Protein ◽  
Ashbya Gossypii ◽  
Wild Type ◽  
Riboflavin Production ◽  
Real Time Quantitative Pcr ◽  
Insertional Mutant ◽  
In The Wild ◽  
Green Fluorescent

ABSTRACT Ashbya gossypii is a natural riboflavin overproducer used in the industrial production of the vitamin. We have isolated an insertional mutant exhibiting higher levels of riboflavin production than the wild type. DNA analysis of the targeted locus in the mutant strain revealed that a syntenic homolog of the Saccharomyces cerevisiae BAS1 gene, a member of the Myb family of transcription factors, was inactivated. Directed gene disruption of AgBAS1 confirmed the phenotype observed for the insertional mutant, and the Δbas1 mutant also showed auxotrophy for adenine and several growth defects, such as a delay in the germination of the spores and an abnormally prolonged trophic phase. Additionally, we demonstrate that the DNA-binding domain of AgBas1p is able to bind to the Bas1-binding motifs in the AgADE4 promoter; we also show a clear nuclear localization of a green fluorescent protein-Bas1 fusion protein. Real-time quantitative PCR analyses comparing the wild type and the Δbas1 mutant revealed that AgBAS1 was responsible for the adenine-mediated regulation of the purine and glycine pathways, since the transcription of the ADE4 and SHM2 genes was virtually abolished in the Δbas1 mutant. Furthermore, the transcription of ADE4 and SHM2 in the Δbas1 mutant did not diminish during the transition from the trophic to the productive phase did not diminish, in contrast to what occurred in the wild-type strain. A C-terminal deletion in the AgBAS1 gene, comprising a hypothetical regulatory domain, caused constitutive activation of the purine and glycine pathways, enhanced riboflavin overproduction, and prolonged the trophic phase. Taking these results together, we propose that in A. gossypii, AgBAS1 is an important transcription factor that is involved in the regulation of different physiological processes, such as purine and glycine biosynthesis, riboflavin overproduction, and growth.

Freeze-substituted fungal cells of Nectria haematococca: A comparison of the macroconidial walls of the adhesion-competent wild type with an adhesion-reduced mutant

1990 ◽  
Vol 48 (3) ◽  
pp. 688-689
Author(s):  
Thecan Caesar-Ton That ◽  
Lynn Epstein
Keyword(s):  
Freeze Substitution ◽  
Uranyl Acetate ◽  
Wild Type ◽  
Nectria Haematococca ◽  
Fruit Extract ◽  
Dialysis Tubing ◽  
Tube Emergence ◽  
Contrast Microscopy ◽  
In The Wild ◽  
Freeze Damage

Nectria haematococca mating population I (anamorph, Fusarium solani) macroconidia attach to its host (squash) and non-host surfaces prior to germ tube emergence. The macroconidia become adhesive after a brief period of protein synthesis. Recently, Hickman et al. (1989) isolated N. haematococca adhesion-reduced mutants. Using freeze substitution, we compared the development of the macroconidial wall in the wild type in comparison to one of the mutants, LEI.Macroconidia were harvested at 1C, washed by centrifugation, resuspended in a dilute zucchini fruit extract and incubated from 0 - 5 h. During the incubation period, wild type macroconidia attached to uncoated dialysis tubing. Mutant macroconidia did not attach and were collected on poly-L-lysine coated dialysis tubing just prior to freezing. Conidia on the tubing were frozen in liquid propane at 191 - 193C, substituted in acetone with 2% OsO4 and 0.05% uranyl acetate, washed with acetone, and flat-embedded in Epon-Araldite. Using phase contrast microscopy at 1000X, cells without freeze damage were selected, remounted, sectioned and post-stained sequentially with 1% Ba(MnO4)2 2% uranyl acetate and Reynold’s lead citrate. At least 30 cells/treatment were examined.

Chemotaxis and Transcription Factor Activation of Wild-Type and CCR6-Transfected RLE-6TN

Pneumologie ◽  
2012 ◽  
Vol 66 (11) ◽  
Author(s):  
K Hoehne ◽  
H Eibel ◽  
M Grimm ◽  
M Idzko ◽  
J Müller-Quernheim ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Wild Type ◽  
Transcription Factor Activation
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