The development of fused− embryos of Drosophila melanogaster

Development ◽  
1985 ◽  
Vol 87 (1) ◽  
pp. 99-114
Author(s):  
Alfonso Martinez-Arias
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Embryonic Development ◽  
Mature Embryo ◽  
Lethal Mutations ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Secondary Consequence

The mutant fused (1–59·5) belongs to a class of lethal mutations in Drosophila melanogaster that produce pattern duplications in every segment of the mature embryo. A study of the embryonic development of fused'− embryos derived horn fused− mothers shows that extensive cell death occurs early in development. This cell death accounts for the smaller size of the segments in fused− embryos. The pattern duplication observed is, probably, a secondary consequence of the pattern deletion.

scholarly journals Phenotype of the Triplo-lethal locus of Drosophila melanogaster and its suppression by hyperoxia

2003 ◽  
Vol 82 (3) ◽  
pp. 163-170 ◽  
Author(s):  
LAURA K. SMOYER ◽  
DOUGLAS R. DORER ◽  
KENNETH W. NICKERSON ◽  
ALAN C. CHRISTENSEN
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Environmental Condition ◽  
Reporter Strain ◽  
First Report ◽  
Extensive Cell Death ◽  
Extensive Cell

The Triplo-lethal locus (Tpl) of Drosophila is both triplo-lethal and haploinsufficient, but the function of the locus is unknown. We have examined Tpl-aneuploid embryos and find that, in both trisomics and monosomics, the midgut shows extensive cell death and the tracheae are abnormal. Shortly thereafter, all tissues die. PCR-based genotyping of individual embryos and larvae show that this phenotype occurs in the trisomics after hatching and in the monosomics before hatching. Weak alleles of the interacting gene Su(Tpl) delay the death of Tpl trisomics, but they still show the same tracheal and midgut phenotypes before dying. Hyperoxia (45% oxygen) partially suppresses the phenotype of Tpl aneuploids, even though the use of a hypoxia reporter strain shows that dying Tpl aneuploids are not hypoxic. This is the first report of a phenotype associated with the Tpl locus and the first report of an environmental condition that suppresses the phenotype.

scholarly journals Cells differentiating into neuroectoderm undergo apoptosis in the absence of functional retinoblastoma family proteins.

1995 ◽  
Vol 129 (3) ◽  
pp. 779-788 ◽  
Author(s):  
R S Slack ◽  
I S Skerjanc ◽  
B Lach ◽  
J Craig ◽  
K Jardine ◽  
...  
Keyword(s):  
Cell Death ◽  
P19 Cells ◽  
Adenovirus E1a ◽  
Genes Encoding ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Early Mouse ◽  
Dying Cells ◽  
Related Proteins ◽  
E1a Protein

The retinoblastoma (RB) protein is present at low levels in early mouse embryos and in pluripotent P19 embryonal carcinoma cells; however, the levels of RB rise dramatically in neuroectoderm formed both in embryos and in differentiating cultures of P19 cells. To investigate the effect of inactivating RB and related proteins p107 and p130, we transfected P19 cells with genes encoding mutated versions of the adenovirus E1A protein that bind RB and related proteins. When these E1A-expressing P19 cells were induced to differentiate into neuroectoderm, there was a striking rise in the expression of c-fos and extensive cell death. The ultrastructural and biochemical characteristics of the dying cells were indicative of apoptosis. The dying cells were those committed to the neural lineages because neurons and astrocytes were lost from differentiating cultures. Cell death was dependent on the ability of the E1A protein to bind RB and related proteins. Our results suggest that proteins of the RB family are essential for the development of the neural lineages and that the absence of functional RB activity triggers apoptosis of differentiating neuroectodermal cells.

Autoimmune bone marrow environment severely inhibits B cell development by inducing extensive cell death and inhibiting proliferation

Autoimmunity ◽  
2012 ◽  
Vol 45 (3) ◽  
pp. 210-217 ◽  
Author(s):  
Shih-En Chang ◽  
Linjie Guo ◽  
Jun Tian ◽  
Yang Liu ◽  
Zhuxiu Guo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Death ◽  
B Cell ◽  
Cell Development ◽  
B Cell Development ◽  
Extensive Cell Death ◽  
Extensive Cell

Calcium ionophore-induced de-encryption of tissue factor in monocytes is associated with extensive cell death

2007 ◽  
Vol 119 (5) ◽  
pp. 621-630 ◽  
Author(s):  
C.E. Henriksson ◽  
O. Klingenberg ◽  
M. Hellum ◽  
K.S. Landsverk ◽  
G.B. Joø ◽  
...  
Keyword(s):  
Cell Death ◽  
Tissue Factor ◽  
Calcium Ionophore ◽  
Extensive Cell Death ◽  
Extensive Cell

scholarly journals Mitogen-independent cell cycle progression in B lymphocytes

2019 ◽  
Author(s):  
Amit Singh ◽  
Matthew H. Spitzer ◽  
Jaimy P. Joy ◽  
Mary Kaileh ◽  
Xiang Qiu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Division ◽  
B Lymphocytes ◽  
Cell Cycle Progression ◽  
Adaptive Immune System ◽  
G1 Phase ◽  
Cycle Progression ◽  
Extensive Cell Death ◽  
Extensive Cell

AbstractThe canonical view of the cell cycle posits that G1 progression signals are essential after each mitosis to enter S phase. A subset of tumor cells bypass this requirement and progress to the next cell division in the absence of continued signaling. B and T lymphocytes of the adaptive immune system undergo a proliferative burst, termed clonal expansion, to generate pools of antigen specific cells for effective immunity. There is evidence that rules for lymphocyte cell division digress from the canonical model. Here we show that B lymphocytes sustain several rounds of mitogen-independent cell division following the first mitosis. Such division is driven by unique characteristics of the post mitotic G1 phase and limited by extensive cell death that can be circumvented by appropriate anti-apoptotic signals. An essential component for continued cell division is Birc5 (survivin), a protein associated with chromosome segregation in G2/M. Our observation provides direct evidence for Pardee’s hypothesis that retention of features of G2M in post-mitotic cells could trigger further cell cycle progression. The partially active G1 phase and propensity for apoptosis that is inherited after each division may permit rapid burst of proliferation and cell death that are hallmarks of immune responses.

scholarly journals ON THE DEVELOPMENT OF ECTOPIC EYES IN DROSOPHILA MELANOGASTER PRODUCED BY THE MUTATION EXTRA EYE (EE)

Genetics ◽  
1985 ◽  
Vol 111 (1) ◽  
pp. 67-88
Author(s):  
William K Baker ◽  
David J Marcey ◽  
M Catharine McElwain
Keyword(s):  
Cell Death ◽  
Larval Instar ◽  
Temperature Shift ◽  
Mirror Image ◽  
Temperature Sensitive ◽  
Cell Counts ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Cell Autonomy ◽  
Ectopic Eyes

ABSTRACT The mutation ee often produces an ectopic eye on the vertex that is a mirror image partial duplication of the normal eye on the ipsilateral side of the head. The pattern of the duplication and a clonal analysis by mitotic recombination indicate that the duplications are of dorsal eye and orbital structures. Large ectopic eyes (more than 100 ommatidia) and their surrounding bristles may be produced without cuticular deficiencies. The penetrance of ee is temperature dependent with penetrance higher (72%) at 25° and 29° than at 19° (43%). Temperature shift experiments show two temperature-sensitive periods: one at midembryogenesis, the other at mid-first larval instar. Microscopic examination of ee late-second and third instar imaginal cephalic discs show no indication of growth of the extra tissue needed to produce the duplication until after mid-third instar. This was confirmed by cell counts of ee and wild-type discs. There is no evidence of differential cell death in the two types of discs at this stage, although much earlier cell death is postulated. Tests for cell autonomy of the mutation by the production of morphogenetic clones suggest nonautonomy. Formation of pattern duplications by mutant genes is discussed in terms of cell death that eliminates whole developmental compartments, restricted cell death that occurs within a compartment, extensive cell death within a compartment and proliferative growth unassociated with cell lethality.

scholarly journals EGF-R dependent regulation of keratinocyte survival

1997 ◽  
Vol 110 (2) ◽  
pp. 113-121 ◽  
Author(s):  
U. Rodeck ◽  
M. Jost ◽  
C. Kari ◽  
D.T. Shih ◽  
R.M. Lavker ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Development ◽  
Growth Factor Receptor ◽  
Human Keratinocytes ◽  
Molecular Control ◽  
Tissue Organization ◽  
Extensive Cell Death ◽  
Dependent Signal ◽  
Extensive Cell ◽  
Normal Human

Tissue organization and maintenance within multicellular organisms is in part dependent on the ability of cells to undergo programmed cell death or apoptosis. Conversely, disruption of cell death pathways often is associated with tumor development. At present, the molecular control of apoptosis in epithelial cells is poorly understood. Here we describe evidence linking epidermal growth factor-receptor (EGF-R) activation to survival of normal human keratinocytes in culture. Inhibition of EGF-R activation by an anti-EGF-R antagonistic monoclonal antibody (mAb 425), followed by detachment of keratinocytes from the substratum, induced extensive death with several features of apoptosis in keratinocyte cultures. Other, non-epithelial normal human cells including melanocytes and fibroblasts, did not show this effect. Similar to EGF-R blockade by mAb 425, inhibition of the EGF-R tyrosine kinase activity using tyrphostin AG1478 resulted in lack of attachment and extensive cell death upon passaging. Attachment to keratinocyte-derived ECM partially resuced mAb 425-treated keratinocytes from cell death, indicating that adhesion-dependent and EGF-R-dependent signal transduction pathways serve partially overlapping but not redundant roles in supporting keratinocyte survival.

scholarly journals Overexpression of UCP2 Protects Thalamic Neurons following Global Ischemia in the Mouse

2008 ◽  
Vol 28 (6) ◽  
pp. 1186-1195 ◽  
Author(s):  
Tomas Deierborg Olsson ◽  
Tadeusz Wieloch ◽  
Sabrina Diano ◽  
Craig H Warden ◽  
Tamas L Horvath ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Damage ◽  
Uncoupling Protein ◽  
Global Ischemia ◽  
Thalamic Nuclei ◽  
Global Brain Ischemia ◽  
Ucp2 Expression ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Global Brain

Uncoupling protein 2 (UCP2) is upregulated in the brain after sublethal ischemia, and overexpression of UCP2 is neuroprotective in several models of neurodegenerative disease. We investigated if increased levels of UCP2 diminished neuronal damage after global brain ischemia by subjecting mice overexpressing UCP2 (UCP2/3tg) and wild-type littermates (wt) to a 12-min global ischemia. The histopathological outcome in the cortex, hippocampus, striatum, and thalamus was evaluated at 4 days of recovery, allowing maturation of the selective neuronal death. Global ischemia led to extensive cell death in the striatum, thalamus, and in the CA1 and CA2, and less-pronounced cell death in the CA3 and dentate gyrus (DG) hippocampal subfields. Histologic damage was significantly lower in the ventral posterolateral VPL and medial VPM thalamic nuclei in UCP2/3tg animals compared with wt. These thalamic regions showed a larger increase in UCP2 expression in UCP2/3tg compared with wt animals relative to the nonprotected DG. In the other regions studied, the histologic damage was lower or equal in UCP2/3tg animals compared with wt. Consequently, neuroprotection in the thalamus correlated with a high expression of UCP2, which is neuroprotective in a number of models of neurodegenerative diseases.

scholarly journals Induction of Rapid Cell Death by an Environmental Isolate of Legionella pneumophila in Mouse Macrophages

2013 ◽  
Vol 81 (9) ◽  
pp. 3077-3088 ◽  
Author(s):  
Lili Tao ◽  
Wenhan Zhu ◽  
Bi-Jie Hu ◽  
Jie-Ming Qu ◽  
Zhao-Qing Luo
Keyword(s):  
Cell Death ◽  
Legionella Pneumophila ◽  
Immune Surveillance ◽  
Human Macrophage ◽  
Aqueous Environment ◽  
Intracellular Replication ◽  
Content Type ◽  
Type Iv ◽  
Extensive Cell Death ◽  
Extensive Cell

ABSTRACTLegionella pneumophila, the etiological agent for Legionnaires' disease, is ubiquitous in the aqueous environment, where it replicates as an intracellular parasite of free-living protozoa. Our understanding ofL. pneumophilapathogenicity is obtained mostly from study of derivatives of several clinical isolates, which employ almost identical virulent determinants to exploit host functions. To determine whether environmentalL. pneumophilaisolates interact similarly with the model host systems, we analyzed intracellular replication of several recently isolated such strains and found that these strains cannot productively grow in bone marrow-derived macrophages of A/J mice, which are permissive for all examined laboratory strains. By focusing on one strain called LPE509, we found that its deficiency in intracellular replication in primary A/J macrophages is not caused by the lack of important pathogenic determinants because this strain replicates proficiently in two protozoan hosts and the human macrophage U937 cell. We also found that in the early phase of infection, the trafficking of this strain in A/J macrophages is similar to that of JR32, a derivative of strain Philadelphia 1. Furthermore, infection of these cells by LPE509 caused extensive cell death in a process that requires the Dot/Icm type IV secretion system. Finally, we showed that the cell death is caused neither by the activation of the NAIP5/NLRC4 inflammasome nor by the recently described caspase 11-dependent pathway. Our results revealed that some environmentalL. pneumophilastrains are unable to overcome the defense conferred by primary macrophages from mice known to be permissive for laboratoryL. pneumophilastrains. These results also suggest the existence of a host immune surveillance mechanism differing from those currently known in responding toL. pneumophilainfection.

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