The pattern of cell death in fushi tarazu, a segmentation gene of Drosophila

Development ◽  
1988 ◽  
Vol 104 (3) ◽  
pp. 447-451 ◽  
Author(s):  
L. Magrassi ◽  
P.A. Lawrence

The pair-rule mutant, fushi tarazu, causes deletion of alternate metameres. Here we show that there is cell death in the mutant which begins at the completion of germ band extension. We map the dying cells in the epidermis; they occur scattered all over those regions that, in the wild type, would form the even-numbered parasegments and are also found in posterior parts of the odd-numbered parasegments. In the affected zones, dying and dividing cells are intermingled; we suggest that cells from these zones may still give descendents that contribute to the larval cuticle. Cell death is not limited to those cells that would normally express ftz+, suggesting that it is some indirect consequence of the abnormal situation in the mutant embryo.

Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1343-1352 ◽  
Author(s):  
L.H. Frank ◽  
C. Rushlow

The amnioserosa is an extraembryonic, epithelial tissue that covers the dorsal side of the Drosophila embryo. The initial development of the amnioserosa is controlled by the dorsoventral patterning genes. Here we show that a group of genes, which we refer to as the U-shaped-group (ush-group), is required for maintenance of the amnioserosa tissue once it has differentiated. Using several molecular markers, we examined amnioserosa development in the ush-group mutants: u-shaped (ush), hindsight (hnt), serpent (srp) and tail-up (tup). Our results show that the amnioserosa in these mutants is specified correctly and begins to differentiate as in wild type. However, following germ-band extension, there is a premature loss of the amnioserosa. We demonstrate that this cell loss is a consequence of programmed cell death (apoptosis) in ush, hnt and srp, but not in tup. We discuss the role of the ush-group genes in maintaining the amnioserosa's viability. We also discuss a possible role for the amnioserosa in germ-band retraction in light of these mutants' unretracted phenotype.


2001 ◽  
Vol 69 (7) ◽  
pp. 4610-4617 ◽  
Author(s):  
Renato L. Santos ◽  
Renée M. Tsolis ◽  
Shuping Zhang ◽  
Thomas A. Ficht ◽  
Andreas J. Bäumler ◽  
...  

ABSTRACT Salmonella enterica serovar Typhimurium causes cell death in bovine monocyte-derived and murine macrophages in vitro by asipB-dependent mechanism. During this process, SipB binds and activates caspase-1, which in turn activates the proinflammatory cytokine interleukin-1β through cleavage. We used bovine ileal ligated loops to address the role of serovar Typhimurium-induced cell death in induction of fluid accumulation and inflammation in this diarrhea model. Twelve perinatal calves had 6- to 9-cm loops prepared in the terminal ileum. They were divided into three groups: one group received an intralumen injection of Luria-Bertani broth as a control in 12 loops. The other two groups (four calves each) were inoculated with 0.75 × 109 CFU of either wild-type serovar Typhimurium (strain IR715) or a sopB mutant per loop in 12 loops. Hematoxylin and eosin-stained sections were scored for inflammation, and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells were detected in situ. Fluid accumulation began at 3 h postinfection (PI). Inflammation was detected in all infected loops at 1 h PI. The area of TUNEL-labeled cells in the wild-type infected loops was significantly higher than that of the controls at 12 h PI, when a severe inflammatory response and tissue damage had already developed. ThesopB mutant induced the same amount of TUNEL-positive cells as the wild type, but it was attenuated for induction of fluid secretion and inflammation. Our results indicate that serovar Typhimurium-induced cell death is not required to trigger an early inflammatory response and fluid accumulation in the ileum.


2004 ◽  
Vol 70 (5) ◽  
pp. 2717-2721 ◽  
Author(s):  
Jennifer Cleveland McEntire ◽  
George M. Carman ◽  
Thomas J. Montville

ABSTRACT The growth of the foodborne pathogen Listeria monocytogenes can be controlled by nisin, an antimicrobial peptide. A spontaneous mutant of L. monocytogenes shows both resistance to nisin and increased acid sensitivity compared to the wild type. Changes in the cell membrane correlated with nisin resistance, but the mechanism for acid sensitivity appears unrelated. When hydrochloric or lactic acid is added to cultures, intracellular ATP levels drop significantly in the mutant (P < 0.01) compared to the results seen with the wild type. Characterization of the F0F1 ATPase, which hydrolyzes ATP to pump protons from the cell cytoplasm, shows that the enzyme is more active in the mutant than in the wild type. These data support a model in which the increased activity of the mutant ATPase upon acid addition depletes the cells' supply of ATP, resulting in cell death.


Development ◽  
1994 ◽  
Vol 120 (7) ◽  
pp. 1829-1837 ◽  
Author(s):  
U. Tepass ◽  
L.I. Fessler ◽  
A. Aziz ◽  
V. Hartenstein

We have studied the embryonic development of Drosophila hemocytes and their conversion into macrophages. Hemocytes derive exclusively from the mesoderm of the head and disperse along several invariant migratory paths throughout the embryo. The origin of hemocytes from the head mesoderm is further supported by the finding that in Bicaudal D, a mutation that lacks all head structures, and in twist snail double mutants, where no mesoderm develops, hemocytes do not form. All embryonic hemocytes behave like a homogenous population with respect to their potential for phagocytosis. Thus, in the wild type, about 80–90% of hemocytes become macrophages during late development. In mutations with an increased amount of cell death (knirps; stardust; fork head), this figure approaches 100%. In contrast, in these mutations, the absolute number of hemocytes does not differ from that in wild type, indicating that cell death does not ‘induce’ the formation of hemocytes. Finally, we show that, in the Drosophila embryo, apoptosis can occur independently of macrophages, since mutations lacking macrophages (Bicaudal D; twist snail double mutants; torso4021) show abundant cell death.


2013 ◽  
Vol 12 (6) ◽  
pp. 913-922 ◽  
Author(s):  
John Mavrianos ◽  
Elizabeth L. Berkow ◽  
Chirayu Desai ◽  
Alok Pandey ◽  
Mona Batish ◽  
...  

ABSTRACTTwo-component signal transduction pathways are one of the primary means by which microorganisms respond to environmental signals. These signaling cascades originated in prokaryotes and were inherited by eukaryotes via endosymbiotic lateral gene transfer from ancestral cyanobacteria. We report here that the nuclear genome of the pathogenic fungusCandida albicanscontains elements of a two-component signaling pathway that seem to be targeted to the mitochondria. TheC. albicanstwo-component response regulator protein Srr1 (stressresponseregulator 1) contains a mitochondrial targeting sequence at the N terminus, and fluorescence microscopy reveals mitochondrial localization of green fluorescent protein-tagged Srr1. Moreover, phylogenetic analysis indicates thatC. albicansSrr1 is more closely related to histidine kinases and response regulators found in marine bacteria than are other two-component proteins present in the fungi. These data suggest conservation of this protein during the evolutionary transition from endosymbiont to a subcellular organelle. We used microarray analysis to determine whether the phenotypes observed with asrr1Δ/Δmutant could be correlated with gene transcriptional changes. The expression of mitochondrial genes was altered in thesrr1Δ/Δnull mutant in comparison to their expression in the wild type. Furthermore, apoptosis increased significantly in thesrr1Δ/Δmutant strain compared to the level of apoptosis in the wild type, suggesting the activation of a mitochondrion-dependent apoptotic cell death pathway in thesrr1Δ/Δmutant. Collectively, this study shows for the first time that a lower eukaryote likeC. albicanspossesses a two-component response regulator protein that has survived in mitochondria and regulates a subset of genes whose functions are associated with the oxidative stress response and programmed cell death (apoptosis).


Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1561-1572 ◽  
Author(s):  
R. Dawes ◽  
I. Dawson ◽  
F. Falciani ◽  
G. Tear ◽  
M. Akam

We describe an unusual Antennapedia class homeobox gene from the grasshopper Schistocerca gregaria (Orthoptera, African Plague Locust). Its sequence is not sufficiently similar to that of any other insect Hom-Hox gene to identify it unambiguously, but short conserved elements suggest a relationship to the segmentation gene fushi-tarazu, (ftz). We term it Sg Dax (divergent Antennapedia class homeobox gene). Antibodies raised against the protein encoded by this gene reveal two phases of expression during embryogenesis. In the early embryo, it is a marker for the posterior part of the forming embryonic primordium, and subsequently for the posterior part of the growing germ band. In older embryos, it labels a subset of neural precursor cells in each trunk segment, very similar to that defined by the expression of fushi tarazu (ftz) in Drosophila. We suggest that Schistocerca Dax and Drosophila ftz are homologous members of a gene family whose members are diverging relatively rapidly, both in terms of sequence and role in early development.


2021 ◽  
Vol 22 (16) ◽  
pp. 9046
Author(s):  
Setsuko Komatsu ◽  
Hisateru Yamaguchi ◽  
Keisuke Hitachi ◽  
Kunihiro Tsuchida ◽  
Yuhi Kono ◽  
...  

To investigate the mechanism of flooding tolerance of soybean, flooding-tolerant mutants derived from gamma-ray irradiated soybean were crossed with parent cultivar Enrei for removal of other factors besides the genes related to flooding tolerance in primary generated mutant soybean. Although the growth of the wild type was significantly suppressed by flooding compared with the non-flooding condition, that of the mutant lines was better than that of the wild type even if it was treated with flooding. A two-day-old mutant line was subjected to flooding for 2 days and proteins were analyzed using a gel-free/label-free proteomic technique. Oppositely changed proteins in abundance between the wild type and mutant line under flooding stress were associated in endoplasmic reticulum according to gene-ontology categorization. Immunoblot analysis confirmed that calnexin accumulation increased in both the wild type and mutant line; however, calreticulin accumulated in only the mutant line under flooding stress. Furthermore, although glycoproteins in the wild type decreased by flooding compared with the non-flooding condition, those in the mutant line increased even if it was under flooding stress. Alcohol dehydrogenase accumulated in the wild type and mutant line; however, this enzyme activity significantly increased and mildly increased in the wild type and mutant line, respectively, under flooding stress compared with the non-flooding condition. Cell death increased and decreased in the wild type and mutant line, respectively, by flooding stress. These results suggest that the regulation of cell death through the fermentation system and glycoprotein folding might be an important factor for the acquisition of flooding tolerance in mutant soybean.


Development ◽  
1989 ◽  
Vol 105 (4) ◽  
pp. 761-767 ◽  
Author(s):  
P.A. Lawrence ◽  
P. Johnston

The first sign of metamerization in the Drosophila embryo is the striped expression of pair-rule genes such as fushi tarazu (ftz) and even-skipped (eve). Here we describe, at cellular resolution, the development of ftz and eve protein stripes in staged Drosophila embryos. They appear gradually, during the syncytial blastoderm stage and soon become asymmetric, the anterior margins of the stripes being sharply demarcated while the posterior borders are undefined. By the beginning of germ band elongation, the eve and ftz stripes have narrowed and become very intense at their anterior margins. The development of these stripes in hairy-, runt-, eve-, ftz- and engrailed- embryos is illustrated. In eve- embryos, the ftz stripes remain symmetric and lack sharp borders. Our results support the hypothesis (Lawrence et al. Nature 328, 440–442, 1987) that individual cells are allocated to parasegments with respect to the anterior margins of the eve and ftz stripes.


Author(s):  
Thecan Caesar-Ton That ◽  
Lynn Epstein

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.


2007 ◽  
Vol 28 (3) ◽  
pp. 897-906 ◽  
Author(s):  
Thomas J. Pohl ◽  
Jac A. Nickoloff

ABSTRACT Homologous recombination (HR) is critical for DNA double-strand break (DSB) repair and genome stabilization. In yeast, HR is catalyzed by the Rad51 strand transferase and its “mediators,” including the Rad52 single-strand DNA-annealing protein, two Rad51 paralogs (Rad55 and Rad57), and Rad54. A Rad51 homolog, Dmc1, is important for meiotic HR. In wild-type cells, most DSB repair results in gene conversion, a conservative HR outcome. Because Rad51 plays a central role in the homology search and strand invasion steps, DSBs either are not repaired or are repaired by nonconservative single-strand annealing or break-induced replication mechanisms in rad51Δ mutants. Although DSB repair by gene conversion in the absence of Rad51 has been reported for ectopic HR events (e.g., inverted repeats or between plasmids), Rad51 has been thought to be essential for DSB repair by conservative interchromosomal (allelic) gene conversion. Here, we demonstrate that DSBs stimulate gene conversion between homologous chromosomes (allelic conversion) by >30-fold in a rad51Δ mutant. We show that Rad51-independent allelic conversion and break-induced replication occur independently of Rad55, Rad57, and Dmc1 but require Rad52. Unlike DSB-induced events, spontaneous allelic conversion was detected in both rad51Δ and rad52Δ mutants, but not in a rad51Δ rad52Δ double mutant. The frequencies of crossovers associated with DSB-induced gene conversion were similar in the wild type and the rad51Δ mutant, but discontinuous conversion tracts were fivefold more frequent and tract lengths were more widely distributed in the rad51Δ mutant, indicating that heteroduplex DNA has an altered structure, or is processed differently, in the absence of Rad51.


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