Fig. 5

Disruption of clock function in klf7^−/− mice. A Functional enrichment analysis of differentially expressed genes (DEGs) in 7-day-old male klf7^−/− mice. These DEGs were mainly enriched in the processes related to circadian rhythms. B Clock mRNA levels measured by qPCR in klf7^−/− mice. C Clock protein levels measured by western blot in klf7^−/− mice. D Validation of the mRNA level of rhythm-related genes by qRT-PCR. E Graph showing the levels of rhythm-related genes, which were restored by administering adeno-associated virus (AAV) mediated overexpression of klf7 in klf7^± mice. F Proposed model of klf7’s activity on regulating circadian rhythm genes in ASD development. Under the basal condition, klf7 can target Clock gene and indirectly regulate downstream rhythmic genes, thus forming a feedback loop with Clock gene to maintain the stability of circadian rhythm system. When klf7 is deficient, dysregulation of circadian rhythm gene disrupts the circadian system and leads to ASD. The data are presented as the mean ± SEM. Statistical analysis (P^* < 0.05 and P^** < 0.01) in (B) and (D) were performed by unpaired t test