#c.elegans

Cracking an Egg

Cell division involves chromosomes being segregated on a protein spindle so each daughter cell receives them equally. In egg cells the spindle forms without chromosome involvement – this study in the C. elegans worm reveals the vital role of an enzyme called ZYG-8 in stabilising such spindles

Read the published research article here

Image by Emily Czajkowski and Sadie Wignall, from work by Emily R. Czajkowski and colleagues

Department of Molecular Biosciences, Northwestern University, Evanston, IL, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in and on the cover of PLOS Genetics, September 2024

In a Spindle

Live imaging and electron tomography in cells of the tiny worm Caenorhabditis elegans (C.elegans for short) reveal fine details of the changes in cell structure occurring during female meiosis – specialised cell division for sexual reproduction to produce egg cells with only one pair of chromosomes. The length of the meiotic spindle (a transient assembly of proteins that forms to segregate chromosomes) is correlated with the length of microtubules – tiny flexible pipes formed of a protein called tubulin – which comprise most of the spindle proteins.

Read the published article here

Image from work by Vitaly Zimyanin and Stefanie Redemann

Department of Molecular Physiology and Biological Physics, University of Virginia School of Medicine, Charlottesville, VA, USA

Image originally published with a Creative Commons Attribution – NonCommercial – NoDerivs (CC BY-NC-ND 4.0)

Small Sacrifices

Molecular mechanisms regulating germ cell death in the research model nematode worm Caenorhabditis elegans. Live-tracking individual germ cells that become egg cells (oocytes) shows that their smaller neighbours are first selectively eliminated probably to help accommodate growth and donate resources

Read the published research article here

Image from work by Tea Kohlbrenner and colleagues

Institute of Molecular Life Sciences, University of Zürich, Zürich, Switzerland

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in PLOS Biology, August 2024

That’ll Do Now

Enzyme called MARC3 blocks further sperm entering eggs within seconds after fertilisation in the model organism C.elegans – insight for fertilisation studies in humans

Read the published research article here

Image from work by Ichiro Kawasaki, Kenta Sugiura and Miyuki Sato, and colleagues

Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, January 2024

Cilia Conservation

Regulation of genes active in nematode worm cilia – sensory structures on many cells – provides insight into the evolution of these highly specialised organelles

Read the published research paper here

Image from work by Rebeca Brocal-Ruiz and colleagues

Developmental Neurobiology Unit, Instituto de Biomedicina de Valencia IBV-CSIC, Valencia, Spain

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in eLife, July 2023

Switched Off

Hidden within our genome are sequences of DNA called transposable elements (TEs) that can move between locations, and potentially disrupt key genes. Our germ cells – precursors of eggs and sperm – have evolved a defence in the form of piwi-interacting RNAs (piRNAs), which silence TEs. But whether piRNAs also silence genes involved in producing germ cells was unclear. Using the nematode worm as a model, researchers found that piRNAs silenced genes involved in sperm formation. In worms with mutated non-functioning piRNAs (bottom), there were more germ cells expressing genes linked to creating sperm (red) compared to a ‘normal’ worm (top). As these worms are hermaphrodites, they need this ‘switch off’ of sperm production to be able to start making egg cells (yellow). This study shows that piRNAs could have wider roles in humans beyond simply silencing TEs.

Written by Sophie Arthur

Image from work by Eric Cornes and colleagues

Mechanisms of Epigenetic Inheritance, Department of Developmental and Stem Cell Biology, Institut Pasteur, UMR 3738, CNRS, Paris, France

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Developmental Cell, January 2022

Starting Sound

The whistle blows and the game starts. Researchers are hoping they too can use a burst of sound to spark a flurry of activity, just on a smaller scale. Previous work showed that it was possible to use ultrasound to activate cells in microscopic worms by adding particular proteins to neurons [brain cells], but repeating the feat in mammal cells proved more difficult. A recent study tested hundreds of human proteins and found one sensitive to an ultrasound frequency well known to be safe for humans. TRPA1 is a protein that responds to the environment to control tiny channels in cells. The team found that when added to human neurons in the lab or living mouse brains (pictured, TRPA1 in red), it can activate neurons in response to ultrasound. This could eventually enable deep brain stimulation or pacemakers in patients without the need for surgically implanted devices.

Written by Anthony Lewis

Image from work by Marc Duque, Corinne A. Lee-Kubl and Yusuf Tufail, and colleagues

Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, La Jolla, CA, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, February 2022

A Worm’s Word

First symptoms of the neurodegenerative disease amyotrophic lateral sclerosis (ALS) include limb weakness and loss of muscle control, worsening as death of brain and nervous system cells progresses. It’s the most common form of motor neuron disease, with an estimated 1,700 people in the UK being diagnosed annually, and has a life expectancy of two to five years. Here, innovative imaging and behaviour quantification techniques are being used to study the molecular mechanisms of ALS in a worm model bearing a gene mutation like that underlying a form of the human disease. Compared to control worms (top) proteins implicated in ALS accumulate in the worm model (red, lower panel). Observing neurodegeneration and locomotor defects in these worms allows comparison with ALS observations in humans. Translating this research into the clinic could provide novel treatments for ALS patients and generating other such worm models could also help unpick the complex molecular basis for a myriad of rare genetic diseases. 

Research in collaboration with the MRC London Institute of Medical Sciences' Behavioural Phenomics group

Written by Daniella Gimbosh

Image from work by Yoshifumi Sonobe and colleagues

The Grossman Institute for Neuroscience, Quantitative Biology, and Human Behavior, University of Chicago, Chicago, IL, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, November 2021