Authors
Roper, R. J., Otte, E., Bratch, E., Robbins, A., Goodlett, C. R.
Abstract
Dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) is a dosage sensitive gene located on human chromosome 21 (Hsa21) that contributes to phenotypes associated with developmental disorders like Down syndrome and DYRK1A haploinsufficiency syndrome. Complete genetic knockout of Dyrk1a from conception is embryonic lethal, presenting a barrier in its study. The mbk-1 gene in Caenorhabditis elegans has been identified as an ortholog to mammalian Dyrk1a, and genetic knockout of mbk-1 in C. elegans is not lethal. We hypothesized that deletion of the mbk-1 gene would alter chemosensory function, learning, and motility in C. elegans, and uncover developmental roles that may inform function of mammalian Dyrk1a. Using behavioral preference index assays, analyses of locomotion, and learning in classical conditioning procedures, an mbk-1 knockout strain of C. elegans, EK228, was characterized to identify potential roles of mbk-1 in development. Preference index assays to assess chemosensory capabilities determined that mbk-1 deletion yielded no detrimental effects. Thrashing and foraging behavior analyses uncovered significant deficits in movement in the EK228 C. elegans, suggesting a role of mbk-1 in locomotion and motility. Lastly, classical conditioning revealed no significant deficits in the abilities of the EK228 strain in forming associative connections between stimuli. Overall, these results imply that EK228 may be a useful model for studying the developmental effects of mbk-1 and implicate the gene in fundamental functions in adaptive movement in the simplified nervous system of C. elegans. Further understanding of this model could provide insight into the early roles of Dyrk1a in mammalian development.
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bioRxiv
The authors list and abstract were imported from bioRxiv on 06 Nov 2025.
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