Cell cycle protein L1 （ccnl1a） is a nuclear protein. As a key regulatory factor of CDK， it regulates the activity of CDK through its periodic expression and jointly regulates alternative splicing with CDK12. To elucidate the physiological function of cell cycle protein L1 （ccnl1a） in the development of vertebrates， this study used CRISPR/cas9 technology to construct a zebrafish ccnl1a knockout model. Phenotypic analysis showed that the mutant exhibited significantly lower body weight， body length， and body height compared to the wild type （P<0.05）， confirming that ccnl1a is a key regulatory factor for growth traits. Whole transcriptome analysis further revealed that upregulated genes included members of the apoptotic pathway dthd1， negative regulators of proliferation pias2， and cell population regulators cgref1； downregulated genes covered metabolic-related factors （fatty acid synthase elovl2， cholesterol pathway genes ebp）， angiogenic factors mydgf， protein transport protein lman1， secretion pathway components spcs2， and sugar metabolism receptors gcgra. This study first revealed an in vivo model the association between ccnl1a deficiency and systemic growth disorders， and based on transcriptome analysis， constructed a cross-pathway regulatory model： that ccnl1a deficiency may coordinate the regulation of activation， proliferation inhibition， and metabolic/suppression functions， jointly leading to growth defects.