Circadian rhythms are endogenous oscillations adapted to environmental factors (Zeitgebers) which allow the biological clock to be adjusted to a 24-hour cycle. The circadian clock is based on clock genes that interact with each other to generate a transcription-translation feedback loop (TTFL). The output produced by the central clock is transmitted through neuronal/neuroendocrine signals throughout the body. Caenorhabditis elegans is a powerful model which offers an extensive set of molecular genetic tools to study the function and interaction of central clock proteins. In this work, we focused on the study of three proteins, LIN-42, KIN-20 and AHA-1, which are homologous to the mammalian and Drosophila clock genes PER, Casein Kinase 1δ/ε and BMAL-1, respectively. We studied how circadian rhythms are affected in strains carrying mutations in putative clock-related proteins, by means of a bioluminescent reporter system. Mutations in the three proteins induced a longer period compared to the wild type strain (close to 24 h): Lin-42 full deletion (26,41 ± 0,47 h, n=32), KIN-20 mutant (26,61 ± 0,69 h, n=39) and AHA-1 mutant (27,14 ± 0,61 h, n=36). In addition, the mutants exhibited a large phase change (> 3 h) when transferred from LD to DD cycle. In summary, our results allow us to obtain a better understanding of the proteins involved in the central clock of the adult nematode.