Figure 3. Collagen XIX is expressed by... | Rockefeller University Press

Figure 3.

$Figure 3. Collagen XIX is expressed by subsets of cortical interneurons. (A) Top genes predicted by EvoCor analysis as being functionally related to mouse col19a1 based on evolutionary history and tissue-wide gene expression patterns. HD, Hamming distance; PCorr, Pearson correlation. (B) Tissue distribution of 40 genes listed in A. (C) >60% of top genes predicted by EvoCor analysis are implicated in contributing to synapse formation or function. (D and E) ISH for col19a1 mRNA in P8 mouse brain. (E) High-magnification image of col19a1 mRNA distribution in visual cortex. Th, dorsal thalamus. Bars, 200 µm. (F) qPCR shows relative levels of col19a1 mRNA expression in vCTX and pfCTX versus dorsal thalamus. Expression levels normalized to gapdh. Data are mean ± SEM; n = 4. *, Differs from thalamic expression by P < 0.0001 by one-way analysis of variance. (G) qPCR shows that col19a1 mRNA expression is developmentally regulated. Expression levels normalized to gapdh. Data are mean ± SEM; n = 3. *, Differs from expression at P21 by P < 0.0001 by one-way analysis of variance. (H–J) ISH reveals that col19a1 is generated by syt1-expressing neurons (H) but not by astrocytes (I) or microglia (J) in P14 mouse cortex. H shows a double ISH experiment, whereas I and J represent ISH-IHC experiments. Bar, 25 µm. (K–N) ISH reveals that col19a1 is generated by GAD67+, Calb+, and Som+ interneurons (K–M) but not Calr+ interneurons (N), as determined by ISH-IHC. (O–Q) Most col19a1-expressing neurons do not generate Parv. Double ISH (O and P) and ISH-IHC (with parv-cre::thy1-stop-yfp tissue; Q) revealed that only a small fraction (if any) of col19a1-expressing neurons generate Parv. Ages of each experiment are indicated in K″–Q″. Bar, 25 µm.$

Collagen XIX is expressed by subsets of cortical interneurons. (A) Top genes predicted by EvoCor analysis as being functionally related to mouse col19a1 based on evolutionary history and tissue-wide gene expression patterns. HD, Hamming distance; PCorr, Pearson correlation. (B) Tissue distribution of 40 genes listed in A. (C) >60% of top genes predicted by EvoCor analysis are implicated in contributing to synapse formation or function. (D and E) ISH for col19a1 mRNA in P8 mouse brain. (E) High-magnification image of col19a1 mRNA distribution in visual cortex. Th, dorsal thalamus. Bars, 200 µm. (F) qPCR shows relative levels of col19a1 mRNA expression in vCTX and pfCTX versus dorsal thalamus. Expression levels normalized to gapdh. Data are mean ± SEM; n = 4. *, Differs from thalamic expression by P < 0.0001 by one-way analysis of variance. (G) qPCR shows that col19a1 mRNA expression is developmentally regulated. Expression levels normalized to gapdh. Data are mean ± SEM; n = 3. *, Differs from expression at P21 by P < 0.0001 by one-way analysis of variance. (H–J) ISH reveals that col19a1 is generated by syt1-expressing neurons (H) but not by astrocytes (I) or microglia (J) in P14 mouse cortex. H shows a double ISH experiment, whereas I and J represent ISH-IHC experiments. Bar, 25 µm. (K–N) ISH reveals that col19a1 is generated by GAD67⁺, Calb⁺, and Som⁺ interneurons (K–M) but not Calr⁺ interneurons (N), as determined by ISH-IHC. (O–Q) Most col19a1-expressing neurons do not generate Parv. Double ISH (O and P) and ISH-IHC (with parv-cre::thy1-stop-yfp tissue; Q) revealed that only a small fraction (if any) of col19a1-expressing neurons generate Parv. Ages of each experiment are indicated in K″–Q″. Bar, 25 µm.