Patterned epidermal cell death in wild-type and segment polarity mutant Drosophila embryos

Development ◽  
1998 ◽  
Vol 125 (17) ◽  
pp. 3427-3436 ◽  
Author(s):  
T.M. Pazdera ◽  
P. Janardhan ◽  
J.S. Minden
Keyword(s):  
Cell Death ◽  
Embryonic Development ◽  
Epidermal Cell ◽  
Time Lapse ◽  
Wild Type ◽  
Segment Polarity ◽  
Genetic Perturbations ◽  
Mutant Phenotypes ◽  
Cell Death Pattern ◽  
Drosophila Embryos

Programmed cell death plays an essential role in the normal embryonic development of Drosophila melanogaster. One region of the embryo where cell death occurs, but has not been studied in detail, is the abdominal epidermis. Because cell death is a fleeting process, we have used time-lapse, fluorescence microscopy to map epidermal apoptosis throughout embryonic development. Cell death occurs in a stereotypically striped pattern near both sides of the segment border and to a lesser extent in the middle of the segment. This map of wild-type cell death was used to determine how cell death patterns change in response to genetic perturbations that affect epidermal patterning. Previous studies have suggested that segment polarity mutant phenotypes are partially the result of increased cell death. Mutations in wingless, armadillo, and gooseberry led to dramatic increases in apoptosis in the anterior of the segment while a naked mutation resulted in a dramatic increase in the death of engrailed cells in the posterior of the segment. These results show that segment polarity gene expression is necessary for the survival of specific rows of epidermal cells and may provide insight into the establishment of the wild-type epidermal cell death pattern.

scholarly journals Deletion of the Dynein Heavy-Chain Gene DYN1 Leads to Aberrant Nuclear Positioning and Defective Hyphal Development in Candida albicans

2004 ◽  
Vol 3 (6) ◽  
pp. 1574-1588 ◽  
Author(s):  
R. Martin ◽  
A. Walther ◽  
J. Wendland
Keyword(s):  
Candida Albicans ◽  
Heavy Chain ◽  
Time Lapse ◽  
Yeast Cells ◽  
Chain Gene ◽  
Wild Type ◽  
Heavy Chain Gene ◽  
Mutant Strains ◽  
Mutant Phenotypes

ABSTRACT Cytoplasmic dynein is a microtubule-associated minus-end-directed motor protein. CaDYN1 encodes the single dynein heavy-chain gene of Candida albicans. The open reading frames of both alleles of CaDYN1 were completely deleted via a PCR-based approach. Cadyn1 mutants are viable but grow more slowly than the wild type. In vivo time-lapse microscopy was used to compare growth of wild-type (SC5314) and dyn1 mutant strains during yeast growth and after hyphal induction. During yeast-like growth, Cadyn1 strains formed chains of cells. Chromosomal TUB1-GFP and HHF1-GFP alleles were used both in wild-type and mutant strains to monitor the orientation of mitotic spindles and nuclear positioning in C. albicans. In vivo fluorescence time-lapse analyses with HHF1-GFP over several generations indicated defects in dyn1 cells in the realignment of spindles with the mother-daughter axis of yeast cells compared to that of the wild type. Mitosis in the dyn1 mutant, in contrast to that of wild-type yeast cells, was very frequently completed in the mother cells. Nevertheless, daughter nuclei were faithfully transported into the daughter cells, resulting in only a small number of multinucleate cells. Cadyn1 mutant strains responded to hypha-inducing media containing l-proline or serum with initial germ tube formation. Elongation of the hyphal tubes eventually came to a halt, and these tubes showed a defect in the tipward localization of nuclei. Using a heterozygous DYN1/dyn1 strain in which the remaining copy was controlled by the regulatable MAL2 promoter, we could switch between wild-type and mutant phenotypes depending on the carbon source, indicating that the observed mutant phenotypes were solely due to deletion of DYN1.

Segment polarity gene interactions modulate epidermal patterning in Drosophila embryos

Development ◽  
1993 ◽  
Vol 119 (2) ◽  
pp. 501-517 ◽  
Author(s):  
A. Bejsovec ◽  
E. Wieschaus
Keyword(s):  
Cell Types ◽  
Epidermal Cells ◽  
Specific Cell ◽  
Wild Type ◽  
Individual Gene ◽  
Segment Polarity Genes ◽  
Segment Polarity ◽  
Drosophila Larva ◽  
Cuticular Structures ◽  
Drosophila Embryos

Each segment of a Drosophila larva shows a precisely organized pattern of cuticular structures, indicating diverse cellular identities in the underlying epidermis. Mutations in the segment polarity genes alter the cuticle pattern secreted by the epidermal cells; these mutant patterns provide clues about the role that each gene product plays in the development of wild-type epidermal pattern. We have analyzed embryos that are multiply mutant for five key patterning genes: wingless, patched, engrailed, naked and hedgehog. Our results indicate that wild-type activity of these five segment polarity genes can account for most of the ventral pattern elements and that their gene products interact extensively to specify the diverse cellular identities within the epidermis. Two pattern elements can be correlated with individual gene action: wingless is required for formation of naked cuticle and engrailed is required for formation of the first row of denticles in each abdominal denticle belt. The remaining cell types can be produced by different combinations of the five gene activities. wingless activity generates the diversity of cell types within the segment, but each specific cell identity depends on the activity of patched, engrailed, naked and hedgehog. These molecules modulate the distribution and interpretation of wingless signalling activity in the ventral epidermal cells and, in addition, each can contribute to pattern through a pathway independent of the wingless signalling pathway.

scholarly journals Echinocandin Drugs Induce Differential Effects in Cytokinesis Progression and Cell Integrity

2021 ◽  
Vol 14 (12) ◽  
pp. 1332
Author(s):  
Natalia Yagüe ◽  
Laura Gómez-Delgado ◽  
M. Ángeles Curto ◽  
Vanessa S. D. Carvalho ◽  
M. Belén Moreno ◽  
...  
Keyword(s):  
Cell Death ◽  
Fluorescence Microscopy ◽  
Fission Yeast ◽  
Mechanism Of Action ◽  
Time Lapse ◽  
Cell Lysis ◽  
Cell Integrity ◽  
Wild Type ◽  
Fungicidal Effect ◽  
Sublethal Concentrations

Fission yeast contains three essential β(1,3)-D-glucan synthases (GSs), Bgs1, Bgs3, and Bgs4, with non-overlapping roles in cell integrity and morphogenesis. Only the bgs4+ mutants pbr1-8 and pbr1-6 exhibit resistance to GS inhibitors, even in the presence of the wild-type (WT) sequences of bgs1+ and bgs3+. Thus, Bgs1 and Bgs3 functions seem to be unaffected by those GS inhibitors. To learn more about echinocandins’ mechanism of action and resistance, cytokinesis progression and cell death were examined by time-lapse fluorescence microscopy in WT and pbr1-8 cells at the start of treatment with sublethal and lethal concentrations of anidulafungin, caspofungin, and micafungin. In WT, sublethal concentrations of the three drugs caused abundant cell death that was either suppressed (anidulafungin and micafungin) or greatly reduced (caspofungin) in pbr1-8 cells. Interestingly, the lethal concentrations induced differential phenotypes depending on the echinocandin used. Anidulafungin and caspofungin were mostly fungistatic, heavily impairing cytokinesis progression in both WT and pbr1-8. As with sublethal concentrations, lethal concentrations of micafungin were primarily fungicidal in WT cells, causing cell lysis without impairing cytokinesis. The lytic phenotype was suppressed again in pbr1-8 cells. Our results suggest that micafungin always exerts its fungicidal effect by solely inhibiting Bgs4. In contrast, lethal concentrations of anidulafungin and caspofungin cause an early cytokinesis arrest, probably by the combined inhibition of several GSs.

Embryonic origin of hemocytes and their relationship to cell death in Drosophila

Development ◽  
1994 ◽  
Vol 120 (7) ◽  
pp. 1829-1837 ◽  
Author(s):  
U. Tepass ◽  
L.I. Fessler ◽  
A. Aziz ◽  
V. Hartenstein
Keyword(s):  
Cell Death ◽  
Embryonic Development ◽  
Absolute Number ◽  
Drosophila Embryo ◽  
Late Development ◽  
Wild Type ◽  
Head Mesoderm ◽  
In The Wild ◽  
Embryonic Origin ◽  
Homogenous Population

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.

scholarly journals Visualization of Melanosome Dynamics within Wild-Type and Dilute Melanocytes Suggests a Paradigm for Myosin V Function In Vivo

1998 ◽  
Vol 143 (7) ◽  
pp. 1899-1918 ◽  
Author(s):  
Xufeng Wu ◽  
Blair Bowers ◽  
Kang Rao ◽  
Qin Wei ◽  
John A. Hammer
Keyword(s):  
Wild Type Mouse ◽  
Time Lapse ◽  
Tail Domain ◽  
Wild Type ◽  
Myosin V ◽  
Transport Models ◽  
Myosin Va ◽  
Cortical Shell ◽  
Mutant Phenotypes

Unlike wild-type mouse melanocytes, where melanosomes are concentrated in dendrites and dendritic tips, melanosomes in dilute (myosin Va−) melanocytes are concentrated in the cell center. Here we sought to define the role that myosin Va plays in melanosome transport and distribution. Actin filaments that comprise a cortical shell running the length of the dendrite were found to exhibit a random orientation, suggesting that myosin Va could drive the outward spreading of melanosomes by catalyzing random walks. In contrast to this mechanism, time lapse video microscopy revealed that melanosomes undergo rapid (∼1.5 μm/s) microtubule-dependent movements to the periphery and back again. This bidirectional traffic occurs in both wild-type and dilute melanocytes, but it is more obvious in dilute melanocytes because the only melanosomes in their periphery are those undergoing this movement. While providing an efficient means to transport melanosomes to the periphery, this component does not by itself result in their net accumulation there. These observations, together with previous studies showing extensive colocalization of myosin Va and melanosomes in the actin-rich periphery, suggest a mechanism in which a myosin Va–dependent interaction of melanosomes with F-actin in the periphery prevents these organelles from returning on microtubules to the cell center, causing their distal accumulation. This “capture” model is supported by the demonstration that (a) expression of the myosin Va tail domain within wild-type cells creates a dilute-like phenotype via a process involving initial colocalization of tail domains with melanosomes in the periphery, followed by an ∼120-min, microtubule-based redistribution of melanosomes to the cell center; (b) microtubule-dependent melanosome movement appears to be damped by myosin Va; (c) intermittent, microtubule-independent, ∼0.14 μm/s melanosome movements are seen only in wild-type melanocytes; and (d) these movements do not drive obvious spreading of melanosomes over 90 min. We conclude that long-range, bidirectional, microtubule-dependent melanosome movements, coupled with actomyosin Va–dependent capture of melanosomes in the periphery, is the predominant mechanism responsible for the centrifugal transport and peripheral accumulation of melanosomes in mouse melanocytes. This mechanism represents an alternative to straightforward transport models when interpreting other myosin V mutant phenotypes.

Apoptosis of the midline glia during Drosophila embryogenesis: a correlation with axon contact

Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 569-578 ◽  
Author(s):  
M.J. Sonnenfeld ◽  
J.R. Jacobs
Keyword(s):  
Cell Death ◽  
Nerve Cord ◽  
Time Course ◽  
Ventral Nerve Cord ◽  
Ectopic Expression ◽  
Wild Type ◽  
Drosophila Embryogenesis ◽  
Quantitative Studies ◽  
The Central Nervous System ◽  
Drosophila Embryos

We have examined cell death within lineages in the midline of Drosophila embryos. Approximately 50% of cells within the anterior, middle and posterior midline glial (MGA, MGM and MGP) lineages died by apoptosis after separation of the commissural axon tracts. Glial apoptosis is blocked in embryos deficient for reaper, where greater than wild-type numbers of midline glia (MG) are present after stage 12. Quantitative studies revealed that MG death followed a consistent temporal pattern during embryogenesis. Apoptotic MG were expelled from the central nervous system and were subsequently engulfed by phagocytic haemocytes. MGA and MGM survival was apparently dependent upon proper axonal contact. In embryos mutant for the commissureless gene, a decrease in axon-glia contact correlated with a decrease in MGA and MGM survival and accelerated the time course of MG death. In embryos mutant for the slit gene, MGA and MGM maintained contact with longitudinally and contralaterally projecting axons and MG survival was comparable to that in wild-type embryos. The initial number of MG within individual ventral nerve cord segments was increased by ectopic expression of the rhomboid gene, without changing axon number. Extra MGA and MGM were eliminated from the ventral nerve cord by apoptosis to restore wild-type numbers of midline glia. Ectopic rhomboid expression also shifted MGA and MGM cell death to an earlier stage of embryogenesis. One possible explanation is that axon-glia contact or communication promotes survival of the MG and that MG death may result from a competition for available axon contact.

Mutations in the clk-1 gene of Caenorhabditis elegans affect developmental and behavioral timing.

Genetics ◽  
1995 ◽  
Vol 139 (3) ◽  
pp. 1247-1259 ◽  
Author(s):  
A Wong ◽  
P Boutis ◽  
S Hekimi
Keyword(s):  
Cell Cycle ◽  
Caenorhabditis Elegans ◽  
Embryonic Development ◽  
Postembryonic Development ◽  
Cycle Period ◽  
Biological Clocks ◽  
Wild Type ◽  
Individual Variations ◽  
In The Wild ◽  
Mutant Phenotypes

Abstract We have identified three allelic, maternal-effect mutations that affect developmental and behavioral timing in Caenorhabditis elegans. They result in a mean lengthening of embryonic and postembryonic development, the cell cycle period and life span, as well as the periods of the defecation, swimming and pumping cycles. These mutants also display a number of additional phenotypes related to timing. For example, the variability in the length of embryonic development is several times larger in the mutants than in the wild type, resulting in the occasional production of mutant embryos developing more rapidly than the most rapidly developing wild-type embryos. In addition, the duration of embryonic development of the mutants, but not of the wild type, depends on the temperature at which their parents were raised. Finally, individual variations in the severity of distinct mutant phenotypes are correlated in a counterintuitive way. For example, the animals with the shortest embryonic development have the longest defecation cycle and those with the longest embryonic development have the shortest defecation cycle. Most of the features affected by these mutations are believed to be controlled by biological clocks, and we therefore call the gene defined by these mutations clk-1, for "abnormal function of biological clocks."

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