The researchers found new clues under the surface of Caenorhabditis, the tiny, transparent worm of Caenorhabditis, which are known as cilia, which help cells sense their surroundings and move materials, to grow in a synchronous way. These structures help worms detect their environment and often grow next to each other in matching pairs. So far, these have been a mystery as they grow. Now, scientists have learned that a protein called ARL13B is involved in tissue and signaling, which plays a key role in managing this structure, and they are called “this pattern” and are called “jog-mounted Cilia-Cilia elongation” – causing two adjacent CILIAs to grow gradually from one another.
Researchers are located at Abdullah Gul University, Merve Gul Turan, Hanife Kantarci, Dr. Sebiha Cevik and Dr. Oktay Kaplan explore this phenomenon and how ARL13B, together with other molecules, supports the co-growth of cilia. Their results were published in the journal Iscience.
Using a special luminescent marker under a microscope (a type of using fluorescence to highlight specific parts of the cell), the scientists tracked how some worms’ sensory nerve cells grew their cilia in matched pairs. In the head of the worm, these projections stretch side by side, and in the tail they form a Y-shaped structure. Even if the actual length of each cilia may vary, the pattern of paired growth remains the same. However, when ARL13B protein is missing, cilia are no longer properly encountered, and in many cases, cilia point in different directions.
Strangely, this misalignment occurs even if the length of the cilium is the same as that of the normal ARL13B worms. This finding suggests that the protein’s role is not just the growth time of cilia length, but also involves helping them maintain their steps. “Our genetic analysis shows that ARL-13 affects the juxtaposed cilia-Cillian extension independently of ciliary length,” Dr. Kaplan said.
Scientists also found that interrupting a group of auxiliary proteins called Bardet-Biedl syndrome protein complexes, a collection of proteins called Bardet-Biedl syndrome protein complexes, could actually improve alignment problems for worms lacking ARL13B. This suggests a possible connection between the work of ARL13B and the changes in the outer layer of cilia, called the ciliary membrane, which is like the skin around the structure. “We suggest that ARL-13 helps juxtapose cilia-Cillian extension, partly through the regulation of the ciliary membrane,” explains Dr. Cevik.
The ARL13B protein was introduced into the worm to allow appropriate alignment of the ciliary pairs. This confirms the importance of this single protein in maintaining cilia coordination. The team also tested other genes known to affect how long cilia grow, such as cyclin-dependent kinase-like 1 (a gene involved in regulating cell activity) and defective dye-filler 5, which play a role in building cilia. However, these genes have no effect on the alignment problem, suggesting that different biological pathways control cilial length and side-by-side growth.
Some combination of genetic changes raises more obvious problems. Delete ARL13B and another gene, Renal Botany 2, a gene associated with renal disease, also affects cilia-alignment alignment. When the third gene, deacetyase 6, which helps regulate protein and cellular structures, is also removed, the cilia grow longer but still fails to align. These results suggest that ARL13B is part of a broader network of proteins that helps maintain proper layout of cilia.
To learn more about the role of the outer surface of cilia, scientists have studied a specific fat-like substance called a lipid marker that usually stays outside the cilia. In the absence of ARL13B, the substance appears inside the cilia, indicating a change in the behavior of the membrane. When the Bardet-Biedl syndrome protein complex is removed in these mutants, the lipid returns to its usual location, supporting the idea that ARL13B helps manage the ciliary membrane.
The discovery of Dr. Kaplan and his colleagues provided strong support for the idea that ARL13B helps organize cilia through changes in the surface of the cilium rather than just its internal structure. Dr. Kaplan believes that other sticky molecules that help cells attach to each other may also help maintain tight bonds between these paired cilia and should be explored in future studies.
Journal Reference
Turan MG, Kantarci H., Cevik S., Kaplan oi “ARL13B regulates cilia-cilia elongation in Bardet-Biedl syndrome protein complex in C. elegans.” Iscience, 2025. Doi:
About the Author
Dr. Sebiha Cevik She is a molecular biologist at Abdullah Gul University in Turkey and a leading researcher who focuses on the cellular mechanisms behind rare genetic diseases. Her work explores how cellular structures like cilia promote human health and development, with particular attention to their role in sensory function and disease. Dr. Cevik has written some influential research in the field and actively directs young biomedical research.
Dr. Oktay Kaplan He is a geneticist at Abdullah Gul University and is known for his work in ciliary biology and cellular tissue. His research investigates how molecular signals coordinate the development and structure of microscopic cellular projections, thereby facilitating our understanding of genetic diseases associated with ciliary dysfunction. Dr. Kaplan also has been building innovative imaging and genetic tools to study field model organisms, e.g. Caenorhabditis elegans.
