Morphology of programmed cell death in the ventral nerve cord of<i>Caenorhabditis elegans</i>larvae

Robertson, Alison M. G.; Thomson, J. N.

doi:10.1242/dev.67.1.89

Cited by 23 publications

(5 citation statements)

References 20 publications

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“…CMS-S pollen collapse presents a plant cell death cytology very like that of animal cells undergoing mitochondria-signaled apoptosis. Collapsed CMS-S pollen reveals condensed cytoplasm containing membrane-bound packets and membranous whorls [31] similar to those described for apoptotic animal cells PCD [21,33]. The DNA breaks and subsequent nuclear fragmentation observed in CMS-S pollen (Fig.…”

Section: Cms-s Pollen Collapse Is a Programmed Cell Death Eventsupporting

confidence: 76%

“…To test this hypothesis, terminal dUTP nick end labeling (TUNEL) assays were performed to examine BCP of CMS-S and N-cytoplasm mito-types for the presence of DNA breaks and nuclear fragmentation (Fig. 2 ), features of apoptotic PCD in animals [ 13 , 33 , 36 ]. Nuclei of the N-cytoplasm YP pollen were TUNEL-negative (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…This cell division marks the transition between the uni-nucleate MSP and bi-cellular pollen (BCP) stages of development [ 32 ]. The morphological features of collapsed CMS-S pollen, including condensed cytoplasm with numerous membrane-bound packets and membranous whorls [ 31 ], are similar to those of animal cells undergoing apoptotic PCD [ 13 , 33 ]. Maize plants produce abundant pollen, and the uni-nucleate MSPs can be physically separated from BCP on sucrose density gradients [ 34 , 35 ].…”

Section: Introductionmentioning

confidence: 99%

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Developmentally regulated mitochondrial biogenesis and cell death competence in maize pollen

et al. 2022

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Background Cytoplasmic male sterility (CMS) is a maternally inherited failure to produce functional pollen that most commonly results from expression of novel, chimeric mitochondrial genes. In Zea mays, cytoplasmic male sterility type S (CMS-S) is characterized by the collapse of immature, bi-cellular pollen. Molecular and cellular features of developing CMS-S and normal (N) cytoplasm pollen were compared to determine the role of mitochondria in these differing developmental fates. Results Terminal deoxynucleotidyl transferase dUTP nick end labeling revealed both chromatin and nuclear fragmentation in the collapsed CMS-S pollen, demonstrating a programmed cell death (PCD) event sharing morphological features with mitochondria-signaled apoptosis in animals. Maize plants expressing mitochondria-targeted green fluorescent protein (GFP) demonstrated dynamic changes in mitochondrial morphology and association with actin filaments through the course of N-cytoplasm pollen development, whereas mitochondrial targeting of GFP was lost and actin filaments were disorganized in developing CMS-S pollen. Immunoblotting revealed significant developmental regulation of mitochondrial biogenesis in both CMS-S and N mito-types. Nuclear and mitochondrial genome encoded components of the cytochrome respiratory pathway and ATP synthase were of low abundance at the microspore stage, but microspores accumulated abundant nuclear-encoded alternative oxidase (AOX). Cytochrome pathway and ATP synthase components accumulated whereas AOX levels declined during the maturation of N bi-cellular pollen. Increased abundance of cytochrome pathway components and declining AOX also characterized collapsed CMS-S pollen. The accumulation and robust RNA editing of mitochondrial transcripts implicated translational or post-translational control for the developmentally regulated accumulation of mitochondria-encoded proteins in both mito-types. Conclusions CMS-S pollen collapse is a PCD event coincident with developmentally programmed mitochondrial events including the accumulation of mitochondrial respiratory proteins and declining protection against mitochondrial generation of reactive oxygen species.

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Section: Cms-s Pollen Collapse Is a Programmed Cell Death Eventsupporting

confidence: 76%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Developmentally regulated mitochondrial biogenesis and cell death competence in maize pollen

et al. 2022

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“…Innate immunity is the evolutionarily ancient part of the immune system that is already present in invertebrates. It is important to note however that in C. elegans, the engulfment and elimination of dying cells are not mediated by professional phagocytes, but instead, they are performed by neighbouring cells, which can be hypodermal, muscle, intestinal and gonadal sheath cells [165,166].…”

Section: Innate Immunity and The Lack Of Direct Pathogen Recognition In C Elegansmentioning

confidence: 99%

Conserved and Distinct Elements of Phagocytosis in Human and C. elegans

Lukácsi

Farkas

Saskői

et al. 2021

IJMS

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Endocytosis provides the cellular nutrition and homeostasis of organisms, but pathogens often take advantage of this entry point to infect host cells. This is counteracted by phagocytosis that plays a key role in the protection against invading microbes both during the initial engulfment of pathogens and in the clearance of infected cells. Phagocytic cells balance two vital functions: preventing the accumulation of cell corpses to avoid pathological inflammation and autoimmunity, whilst maintaining host defence. In this review, we compare elements of phagocytosis in mammals and the nematode Caenorhabditis elegans. Initial recognition of infection requires different mechanisms. In mammals, pattern recognition receptors bind pathogens directly, whereas activation of the innate immune response in the nematode rather relies on the detection of cellular damage. In contrast, molecules involved in efferocytosis—the engulfment and elimination of dying cells and cell debris—are highly conserved between the two species. Therefore, C. elegans is a powerful model to research mechanisms of the phagocytic machinery. Finally, we show that both mammalian and worm studies help to understand how the two phagocytic functions are interconnected: emerging data suggest the activation of innate immunity as a consequence of defective apoptotic cell clearance.

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“…The epidermis of C. elegans is a one-layered epithelium that encases the entire animal ( Chisholm and Hardin, 2005 ) to protect it from extrinsic factors ( Pujol et al, 2008 ). Besides being a barrier, during mid-embryogenesis, it regulates morphogenetic processes like embryonic elongation ( Priess and Hirsh, 1986 ; Williams-Masson et al, 1997 ; Costa et al, 1998 ), cell and axon guidance ( Hedgecock et al, 1990 ), it secretes basement membrane material that separates it from underlying body wall muscles ( Francis and Waterston, 1991 ), and eliminates apoptotic cells and synapses via phagocytosis ( Robertson and Thomson, 1982 ; Chung et al, 2000 ). Importantly, epidermal cells provide the force that drives body elongation ( Priess and Hirsh, 1986 ; Shelton et al, 1999 ; Wissmann et al, 1999 ; Piekny et al, 2003 ; Gally et al, 2009 ; Vuong-Brender et al, 2016 ; Shaye and Soto, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

A Maternal-Effect Toxin Affects Epithelial Differentiation and Tissue Mechanics in Caenorhabditis elegans

Lehmann

Pohl

2021

Front. Cell Dev. Biol.

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Selfish genetic elements that act as post-segregation distorters cause lethality in non-carrier individuals after fertilization. Two post-segregation distorters have been previously identified in Caenorhabditis elegans, the peel-1/zeel-1 and the sup-35/pha-1 elements. These elements seem to act as modification-rescue systems, also called toxin/antidote pairs. Here we show that the maternal-effect toxin/zygotic antidote pair sup-35/pha-1 is required for proper expression of apical junction (AJ) components in epithelia and that sup-35 toxicity increases when pathways that establish and maintain basal epithelial characteristics, die-1, elt-1, lin-26, and vab-10, are compromised. We demonstrate that pha-1(e2123) embryos, which lack the antidote, are defective in epidermal morphogenesis and frequently fail to elongate. Moreover, seam cells are frequently misshaped and mispositioned and cell bond tension is reduced in pha-1(e2123) embryos, suggesting altered tissue material properties in the epidermis. Several aspects of this phenotype can also be induced in wild-type embryos by exerting mechanical stress through uniaxial loading. Seam cell shape, tissue mechanics, and elongation can be restored in pha-1(e2123) embryos if expression of the AJ molecule DLG-1/Discs large is reduced. Thus, our experiments suggest that maternal-effect toxicity disrupts proper development of the epidermis which involves distinct transcriptional regulators and AJ components.

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Morphology of programmed cell death in the ventral nerve cord ofCaenorhabditis eleganslarvae

Cited by 23 publications

References 20 publications

Developmentally regulated mitochondrial biogenesis and cell death competence in maize pollen

Developmentally regulated mitochondrial biogenesis and cell death competence in maize pollen

Conserved and Distinct Elements of Phagocytosis in Human and C. elegans

A Maternal-Effect Toxin Affects Epithelial Differentiation and Tissue Mechanics in Caenorhabditis elegans

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