A Keller-Segel model for C elegans L1 aggregation.

We describe a mathematical model for the aggregation of starved first-stage C elegans larvae (L1s). We propose that starved L1s produce and respond chemotactically to two labile diffusible chemical signals, a short-range attractant and a longer range repellent. This model takes the mathematical form of three coupled partial differential equations, one that describes the movement of the worms and one for each of the chemical signals.

The FMRFamide Neuropeptide FLP-20 Acts as a Systemic Signal for Starvation Responses in .

Most animals face frequent periods of starvation throughout their entire life and thus need to appropriately adjust their behavior and metabolism during starvation for their survival. Such adaptive responses are regulated by a complex set of systemic signals, including hormones and neuropeptides. While much progress has been made in identifying pathways that regulate nutrient-excessive states, it is still incompletely understood how animals systemically signal their nutrient-deficient states.

Modelling the ballistic-to-diffusive transition in nematode motility reveals variation in exploratory behaviour across species.

A quantitative understanding of organism-level behaviour requires predictive models that can capture the richness of behavioural phenotypes, yet are simple enough to connect with underlying mechanistic processes. Here, we investigate the motile behaviour of nematodes at the level of their translational motion on surfaces driven by undulatory propulsion. We broadly sample the nematode behavioural repertoire by measuring motile trajectories of the canonical laboratory strain Caenorhabditis elegans N2 as well as wild strains and distant species.

Starvation-induced collective behavior in C. elegans.

We describe a new type of collective behavior in C. elegans nematodes, aggregation of starved L1 larvae. Shortly after hatching in the absence of food, L1 larvae arrest their development and disperse in search for food.

An opioid-like system regulating feeding behavior in C. elegans.

Neuropeptides are essential for the regulation of appetite. Here we show that neuropeptides could regulate feeding in mutants that lack neurotransmission from the motor neurons that stimulate feeding muscles. We identified nlp-24 by an RNAi screen of 115 neuropeptide genes, testing whether they affected growth.

Regulation of synaptic transmission at the Caenorhabditis elegans M4 neuromuscular junction by an antagonistic relationship between two calcium channels.

In wild-type Caenorhabditis elegans, the synapse from motor neuron M4 to pharyngeal terminal bulb (TB) muscles is silent, and the muscles are instead excited by gap junction connections from adjacent muscles. An eat-5 innexin mutant lacking this electrical connection has few TB contractions and is unable to grow well on certain foods. We showed previously that this defect can be overcome by activation of the M4 → TB synapse.

A model of the effect of uncertainty on the C elegans L2/L2d decision.

At the end of the first larval stage, the C elegans larva chooses between two developmental pathways, an L2 committed to reproductive development and an L2d, which has the option of undergoing reproductive development or entering the dauer diapause. I develop a quantitative model of this choice using mathematical tools developed for pricing financial options. The model predicts that the optimal decision must take into account not only the expected potential for reproductive growth, but also the uncertainty in that expected potential.

Density dependence in Caenorhabditis larval starvation.

Availability of food is often a limiting factor in nature. Periods of food abundance are followed by times of famine, often in unpredictable patterns. Reliable information about the environment is a critical ingredient of successful survival strategy.

The pharynx of the nematode C. elegans: A model system for the study of motor control.

Motor control is a complex process that requires interplay among the nervous system, muscles and environment. The simple anatomy, well-characterized muscle movements and ample resources for molecular and cellular dissection make the pharynx of the nematode C. elegans an attractive model system for the study of motor control.

The jaw of the worm: GTPase-activating protein EAT-17 regulates grinder formation in Caenorhabditis elegans.

Constitutive transport of cellular materials is essential for cell survival. Although multiple small GTPase Rab proteins are required for the process, few regulators of Rabs are known. Here we report that EAT-17, a novel GTPase-activating protein (GAP), regulates RAB-6.

The geometry of locomotive behavioral states in C. elegans.

We develop a new hidden Markov model-based method to analyze C elegans locomotive behavior and use this method to quantitatively characterize behavioral states. In agreement with previous work, we find states corresponding to roaming, dwelling, and quiescence. However, we also find evidence for a continuum of intermediate states.

Recognition of familiar food activates feeding via an endocrine serotonin signal in Caenorhabditis elegans.

Familiarity discrimination has a significant impact on the pattern of food intake across species. However, the mechanism by which the recognition memory controls feeding is unclear. Here, we show that the nematode Caenorhabditis elegans forms a memory of particular foods after experience and displays behavioral plasticity, increasing the feeding response when they subsequently recognize the familiar food.

Appetite Control: worm's-eye-view.

Food is important to any animal, and a large part of the behavioral repertoire is concerned with ensuring adequate nutrition. Two main nutritional sensations, hunger and satiety, produce opposite behaviors. Hungry animals seek food, increase exploratory behavior and continue feeding once they encounter food.

NSBP-1 mediates the effects of cholesterol on insulin/IGF-1 signaling in Caenorhabditis elegans.

Nematode sterol-binding protein 1 (NSBP-1) is a homolog of nucleosome assembly protein 1 in mammals that is expressed widely in Caenorhabditis elegans. NSBP-1 mutants are biologically lethal, demonstrating the significance of the gene in growth and development. We investigated how cholesterol influences the insulin signaling pathway through this novel sterol-binding protein in C.

C. elegans feeding.

C. elegans feeding depends on the action of the pharynx, a neuromuscular pump that joins the mouth to the intestine. The pharyngeal muscle captures food-bacteria-and transports it back to the intestine.

Serotonin activates overall feeding by activating two separate neural pathways in Caenorhabditis elegans.

Food intake in the nematode Caenorhabditis elegans requires two distinct feeding motions, pharyngeal pumping and isthmus peristalsis. Bacteria, the natural food of C. elegans, activate both feeding motions (Croll, 1978; Horvitz et al.

Laser microsurgery in Caenorhabditis elegans.

Laser killing of cell nuclei has long been a powerful means of examining the roles of individual cells in C. elegans. Advances in genetics, laser technology, and imaging have further expanded the capabilities and usefulness of laser surgery.

Hox and a newly identified E2F co-repress cell death in Caenorhabditis elegans.

The development of an organism depends on individual cells receiving and executing their specific fates, although how this process is regulated remains largely unknown. Here, we identify a mechanism by which a specific cell fate, apoptosis, is determined through the cooperative efforts of Hox and E2F proteins. E2F transcription factors are critical, conserved regulators of the cell cycle and apoptosis.

Caenorhabditis elegans behavioral genetics: where are the knobs?

Thousands of behavioral mutants of Caenorhabditis elegans have been studied. I suggest a set of criteria by which some genes important in the evolution of behavior might be recognized, and identify neuropeptide signaling pathways as candidates.

Two size-selective mechanisms specifically trap bacteria-sized food particles in Caenorhabditis elegans.

Caenorhabditis elegans is a filter feeder: it draws bacteria suspended in liquid into its pharynx, traps the bacteria, and ejects the liquid. How pharyngeal pumping simultaneously transports and filters food particles has been poorly understood. Here, we use high-speed video microscopy to define the detailed workings of pharyngeal mechanics.

Death-associated protein kinase (DAPK) and signal transduction: fine-tuning of autophagy in Caenorhabditis elegans homeostasis.

Autophagy is an evolutionarily conserved lysosomal pathway used to degrade and recycle long-lived proteins and cytoplasmic organelles. This homeostatic ability makes autophagy an important pro-survival mechanism in response to several stresses, such as nutrient starvation, hypoxia, damaged mitochondria, protein aggregation and pathogens. However, several recent studies have highlighted that autophagy also acts as a pro-death mechanism.

Latrophilin signaling links anterior-posterior tissue polarity and oriented cell divisions in the C. elegans embryo.

Understanding the mechanisms that coordinate the orientation of cell division planes during embryogenesis and morphogenesis is a fundamental problem in developmental biology. Here we show that the orphan receptor lat-1, a homolog of vertebrate latrophilins, plays an essential role in the establishment of tissue polarity in the C. elegans embryo.

Systemic regulation of autophagy in Caenorhabditis elegans.

When no supply of environmental nutrients is available, cells induce autophagy, thereby generating a source of emergency metabolic substrates and energy to maintain the basal cellular activity needed for survival. This autophagy response to starvation has been well characterized in various multicellular organisms, including worms, flies and mice. Although prosurvival effects of autophagy in response to starvation are well known in animals, the mechanisms by which animals regulate and coordinate autophagy systemically remain elusive.

Systemic regulation of starvation response in Caenorhabditis elegans.

When the supply of environmental nutrients is limited, multicellular animals can make both physiological and behavioral changes so as to cope with nutrient starvation. Although physiological and behavioral effects of starvation are well known, the mechanisms by which animals sense starvation systemically remain elusive. Furthermore, what constituent of food is sensed and how it modulates starvation response is still poorly understood.