EOR-1/PLZF-regulated WAH-1/AIF sequentially promotes early and late stages of non-apoptotic corpse removal.

Unlabelled: Programmed cell death (PCD) is a crucial genetically-encoded and evolutionarily-conserved process for development and homeostasis. We previously identified a genetically non-apoptotic, highly ordered, and stereotyped killing program called Compartmentalized Cell Elimination (CCE) in the tail-spike epithelial cell (TSC). Here we identify the transcription factor EOR-1/PLZF as promoting CCE.

Neurodegeneration-related genes influence pharyngeal activity.

Pharyngeal pumping and its reduction following mechanical insult are well-studied behaviors. Here, we assessed new applications of pharyngeal pumping assays in the study of neurodegenerative disease and psychiatric illness. We examined five genes implicated in two forms of neurodegeneration, Hereditary Spastic Paraplegia (HSPs) and Alzheimer's Disease (AD), for both baseline pharyngeal pumping and the depressive response after touch stimulus.

Apoptosis and beyond: A new era for programmed cell death in Caenorhabditis elegans.

Programmed cell death (PCD) is crucial for normal development and homeostasis. Our first insights into the genetic regulation of apoptotic cell death came from in vivo studies in the powerful genetic model system of C. elegans.

Repurposing the Killing Machine: Non-canonical Roles of the Cell Death Apparatus in Neurons.

Here we highlight the increasingly divergent functions of the cell elimination genes in the nervous system, beyond their well-documented roles in cell dismantling and removal. We describe relevant background on the nervous system together with the apoptotic cell death and engulfment pathways, highlighting pioneering work in . We discuss in detail the unexpected, atypical roles of cell elimination genes in various aspects of neuronal development, response and function.

BLMP-1 promotes developmental cell death in C. elegans by timely repression of ced-9 transcription.

Programmed cell death (PCD) is a common cell fate in metazoan development. PCD effectors are extensively studied, but how they are temporally regulated is less understood. Here, we report a mechanism controlling tail-spike cell death onset during Caenorhabditis elegans development.

The developmental and physiological roles of phagocytosis in Caenorhabditis elegans.

Phagocytosis is an essential process by which cellular debris and pathogens are cleared from the environment. Cells extend their plasma membrane to engulf objects and contain them within a limiting membrane for isolation from the cytosol or for intracellular degradation in phagolysosomes. The basic mechanisms of phagocytosis and intracellular clearance are well conserved between animals.

Cell death in animal development.

Cell death is an important facet of animal development. In some developing tissues, death is the ultimate fate of over 80% of generated cells. Although recent studies have delineated a bewildering number of cell death mechanisms, most have only been observed in pathological contexts, and only a small number drive normal development.

EFF-1 fusogen promotes phagosome sealing during cell process clearance in Caenorhabditis elegans.

Phagocytosis of dying cells is critical in development and immunity. Although proteins for recognition and engulfment of cellular debris following cell death are known, proteins that directly mediate phagosome sealing are uncharacterized. Furthermore, whether all phagocytic targets are cleared using the same machinery is unclear.

Anoxia-reoxygenation regulates mitochondrial dynamics through the hypoxia response pathway, SKN-1/Nrf, and stomatin-like protein STL-1/SLP-2.

Many aerobic organisms encounter oxygen-deprived environments and thus must have adaptive mechanisms to survive such stress. It is important to understand how mitochondria respond to oxygen deprivation given the critical role they play in using oxygen to generate cellular energy. Here we examine mitochondrial stress response in C.

Neurite sprouting and synapse deterioration in the aging Caenorhabditis elegans nervous system.

Caenorhabditis elegans is a powerful model for analysis of the conserved mechanisms that modulate healthy aging. In the aging nematode nervous system, neuronal death and/or detectable loss of processes are not readily apparent, but because dendrite restructuring and loss of synaptic integrity are hypothesized to contribute to human brain decline and dysfunction, we combined fluorescence microscopy and electron microscopy (EM) to screen at high resolution for nervous system changes. We report two major components of morphological change in the aging C.

Hypoxia regulates glutamate receptor trafficking through an HIF-independent mechanism.

Oxygen influences behaviour in many organisms, with low levels (hypoxia) having devastating consequences for neuron survival. How neurons respond physiologically to counter the effects of hypoxia is not fully understood. Here, we show that hypoxia regulates the trafficking of the glutamate receptor GLR-1 in C.