Fig 2: The levels of Arc and Syt1 mRNA in different hippocampal subregions in CD-1 mice. (A,B) Arc mRNA, and (C,D) Syt1 mRNA levels in different hippocampal subregions (CA1, CA3, and DG) in the different treatment groups at 3 months (3 M) (A,C) and 15 months (15 M) (B,D) of age. Error bars = SEM. *P < 0.05, **P < 0.01 compared with the control group; $P < 0.05, $$P < 0.01 compared with the CON + S group; #P < 0.05, ##P < 0.01 compared with the LPS group. CA, cornu ammonis; DG, dentate gyrus; CON, untreated control group; LPS, lipopolysaccharide treatment group; S, group of mice exposed to stress.

Fig 3: Association between the neuronal gene ARC and EMT. (a) ARC and CDH1 expression in six CRC cell lines (DLD-1, Caco2, HT29, RKO, SW480, and HCT116). Red boxes indicate cell lines with relatively high expression of ARC. All experiments were conducted in triplicate. Error bars show standard errors of the mean. (b) Alteration of CDH1 and ZEB1 expression by knockdown of ARC using shRNAs in western blot analysis. Results of ZEB1 were shown from different membranes using the same samples. Quantification of blots and full-length blots are presented in Supplementary Fig. 6b, c and Supplementary Fig. 11a, respectively. (c) Immunocytochemistry of CDH1 and ARC in SW480 cells expressing sh-NC and sh-ARC. Experiments were conducted in triplicate. Scale bars indicate 50 µm. EMT epithelial–mesenchymal transition, CRC colorectal cancer, Sh short hairpin, NC negative control.

Fig 4: Arc Limits the Emergence of Binocular Neurons Early in Development(A) Representative images from two-photon recording of visually evoked calcium responses in Arc KO mice.(B) Percentage of visually responsive neurons that are monocular or binocular in Arc KO mice across age.(C) ODI of the total visually responsive neuron population in Arc KO mice.(D) ODI of binocular neurons in Arc KO mice.(E) Percentage of visually responsive neurons that are monocular or binocular in P30 WT and Arc KO mice.(F) ODI of the neuronal population in P30 WT and Arc KO mice.(G) ODI in binocular neurons of P30 WT and Arc KO mice.(H) HBI of responses in binocular neurons of P30 WT and Arc KO mice.(I) OSI of contralateral responses in binocular neurons of P30 WT and Arc KO mice.(J) DSI of contralateral responses in binocular neurons of P30 WT and Arc KO mice (*p < 0.05 indicates a significant difference between groups; #p < 0.05 indicates a significant difference within a group from the expected mean; error bars represent standard error of the mean; open circles indicate a data point from an individual mouse; n = number of animals for all statistics).See also Figure S3.

Fig 5: Redistribution of AMPAR GluA1 subunit during HSV-1 infection is independent of Arc expression. (A) H4 cells stably expressing either the shRNA to luciferase (H4 shRNA-Luc) used as a control or the shRNA to Arc (H4 shRNA-Arc) to achieve silencing of Arc knockdown (KD) were infected with HSV-1 (MOI = 10) during 8 hpi. Then, GluA1 subunit and ICP8 were immunodetected with specific antibodies followed of secondary antibodies couple to Alexa Fluor 488 and 647, respectively. Phalloidin staining was coupled with Alexa Fluor 594 dye and Nuclei stained with DAPI. Scale bar corresponds to 10 µm. Magnification 630×. The boxes inserted show a zoom capture of the indicated areas. (B) Total protein extracts of H4 shRNA-Luc and H4 shRNA-Arc were analyzed by immunoblot with antibodies to the proteins Arc and GADPH. The results shown are representative of three independent experiments.