3 Papers found (0.007 seconds)

Barsi-Rhyne, Ben et al. (2013) International Worm Meeting "UNC-116/KHC Acts with UNC-6/Netrin and UNC-40/DCC to Maintain Sensory Neuron Position in Caenorhabditis elegans."

VanHoven, Miri, Thomas, Anthony, Barsi-Rhyne, Ben, Park, Joori, Jarecki, Jessica, Bremer, Martina, Miller, Kristine, Vargas, Christopher

[

International Worm Meeting,

2013]

The organization of neurons and the maintenance of that arrangement are critical to brain function. Failure of these processes in humans can lead to severe birth defects, mental retardation, and epilepsy. Several kinesins have been shown to play important roles in cell migration in vertebrate systems, but few upstream and downstream pathway members have been identified. Here, we report that the C. elegans Kinesin-1 Heavy Chain (KHC)/KIF5 ortholog UNC-116 functions to maintain neuronal cell body position of the PHB sensory neurons. We find that UNC-116/KHC acts in part with the cell and axon migration molecules UNC-6/Netrin and UNC-40/DCC in this process, but in parallel to SAX-3/Robo. We have also identified several UNC-116/KHC interactors that are required for this process, including the cargo receptor UNC-33/CRMP2, the cargo adaptor protein UNC-76/FEZ and its regulator UNC-51/ULK, and the cargo molecule UNC-69/SCOCO. In addition, we have identified two actin regulators required for this process: UNC-44/Ankyrin and UNC-34/Enabled. Interestingly, all of these genes also act in cell migration and/or axon outgrowth; however, many proteins that function in these processes do not affect PHB position. UNC-116/KHC appears to act in parallel to previously described adhesive mechanisms involving SAX-7/L1CAM and DGN-1/Dystroglycan. Our findings suggest an active UNC-116/KHC-mediated pathway may direct a posterior migration required to maintain proper PHB cell body position and identify several genes required for proper PHB position.

Martina Machackova et al. (2006) European Worm Meeting "NHR-25 Role in the Seam Cell Differentiation in C. elegans"

Masako ASAHINA, Marek JINDRA, Martina Machackova, Marie SILHANKOVA

[

European Worm Meeting,

2006]

Martina Machackova1, Marie Silhankova1, Marek Jindra and Masako Asahina. Epidermal cell differentiation involves dynamic cell shape changes, important for animal development. During the postembryonic development of Caenorhabditis elegans, most of the stem epidermal seam cells asymmetrically divide and their anterior daughters fuse with the surrounding hyp syncytium, thus creating gaps between the seam stem cells. After each asymmetric division that separates them, the seam cells actively bridge over the gaps to renew their mutual contacts via adherens junctions. The seam cell contacts are important for further epidermal differentiation but the mechanism underlying their renewal is still unknown. We and others have previously shown that the conserved nuclear receptor NHR-25 is necessary for the seam cells to restore contacts after the asymmetric divisions occurring during each larval stage: attenuated NHR-25 function leaves the seam cells round and isolated. nhr-25(RNAi) adults consequently exhibit extra seam cells, indicating that the proper cell fate decision in these epidermal stem cells has been perturbed. NHR-25 might be required either in the seam cells or in the hyp syncytium. Since NHR-25 is highly expressed in the seam cells, its action could be autonomous to these cells. To test this hypothesis, we took an approach of a tissue-specific RNAi system. We have utilized the seam cell-specific promoter (SCM), which is typically used as a seam cell marker, to express a hairpin-loop of nhr-25 RNA in transgenic worms. Independent lines of these transgenic adults show extra seam cells, similar to the effect of nhr-25 RNAi delivered by injection. Although NHR-25 may play a role also in the hyp syncytium, this result suggests that NHR-25 is autonomously required in the seam cells.. Supported by projects Z60220518 (GAAV), 524/03/H133 (GACR) and 6007665801 from the Czech Ministry of Education

Munoz-Lobato, Fernando et al. (2021) International Worm Meeting "Sleep is required for odor exposure to consolidate memory and remodel olfactory synapses."

[

International Worm Meeting,

2021]

Sleep is not only an essential function of humans but remains conserved across metazoans. Here we demonstrate that wild-type C. elegans sleep after repeated odor trainings This provides us with a platform to dissect how sleep affects memory at a synaptic resolution. We identified that sleep immediately after training is required for the animal to retain a long-term memory of the odor. We found that if animals do not sleep in the first two hours after training, memory is not consolidated. After identifying the neurons that are required for the memory, we show that the sensory-interneuron connections within the circuit are downscaled after sleep. Therefore, we found a time-specific requirement of sleep that modulates synaptic downscaling to preserve memory. Conversely, lack of sleep post-training erases the long-term memory and destabilizes the synaptic downscaling, indicating that modulating the amount of sleep is sufficient to modulate memory. These results make C. elegans an excellent tool to ask what molecular mechanisms, cell biological processes and circuit level reorganizations are engaged during sleep to promote memory. This understanding will provide insights into the functions of sleep that contributes to our health and well-being.