Dataset Information

Illuminating the Function of the Orphan Transporter, SLC22A10 in Humans and Other Primates

ABSTRACT: HEK293 Flp-In cells were transfected transiently with various SLC22A10 orthologs, including human, chimpanzee, and the mutations to proline or leucine at position 220. After 72 hours of transfection, cell pellets were collected. The quantification was performed on both HEK293 cells and HEK293cells expressing the different SLC22A10 orthologs and mutations

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Merve Ceylan

LAB HEAD: Per Artursson

PROVIDER: PXD047102 | Pride | 2024-04-09

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	Experimental_Design.xlsx	Xlsx
	SLC22A10_TPA_220322_LysC_S1.raw	Raw
	SLC22A10_TPA_220322_LysC_S2.raw	Raw
	SLC22A10_TPA_220322_LysC_S3.raw	Raw
	SLC22A10_TPA_220322_LysC_S4.raw	Raw

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Illuminating the Function of the Orphan Transporter, SLC22A10 in Humans and Other Primates.

Yee Sook Wah SW Ferrández-Peral Luis L Alentorn Pol P Fontsere Claudia C Ceylan Merve M Koleske Megan L ML Handin Niklas N Artegoitia Virginia M VM Lara Giovanni G Chien Huan-Chieh HC Zhou Xujia X Dainat Jacques J Zalevsky Arthur A Sali Andrej A Brand Colin M CM Capra John A JA Artursson Per P Newman John W JW Marques-Bonet Tomas T Giacomini Kathleen M KM

Research square 20230914

SLC22A10 is classified as an orphan transporter with unknown substrates and function. Here we describe the discovery of the substrate specificity and functional characteristics of SLC22A10. The human SLC22A10 tagged with green fluorescent protein was found to be absent from the plasma membrane, in contrast to the SLC22A10 orthologs found in great apes. Estradiol-17β-glucuronide accumulated in cells expressing great ape SLC22A10 orthologs (over 4-fold, p<0.001). In contrast, human SLC22A10 displa ...[more]

PMID: 37790518

Publication: 1/2

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Project description:Human Accelerated Regions (HARs) are highly conserved across species but exhibit a significant excess of human-specific sequence changes, suggesting they may have gained novel functions in human evolution. HARs include gene regulatory elements with human-specific activity and have been implicated in the evolution of the human brain. However, our understanding of how HARs contributed to uniquely human features of the brain is hindered by a lack of insight into the genes and pathways that HARs regulate. It is unknown whether HARs acted by altering the expression of gene targets conserved between HARs and their chimpanzee orthologs or by gaining new gene targets in human, a mechanism termed enhancer hijacking. We generated a high-resolution map of chromatin interactions for 1,590 HARs and their orthologs in human and chimpanzee neural stem cells (NSCs) to comprehensively identify gene targets in both species. HARs and their chimpanzee orthologs targeted a conserved set of 2,963 genes enriched for neurodevelopmental processes including neurogenesis and synaptic transmission. Changes in HAR enhancer activity were correlated with changes in conserved gene target expression. Conserved targets were enriched among genes differentially expressed between human and chimpanzee NSCs or between human and non-human primate developing and adult brain. Species-specific HAR gene targets did not converge on known biological functions and were not significantly enriched among differentially expressed genes, suggesting that most HARs did not alter gene expression via enhancer hijacking. HAR gene targets, including differentially expressed targets, also showed cell type-specific expression patterns in the developing human brain, notably in outer radial glia, which are hypothesized to contribute to human cortical expansion. Our findings support that HARs influenced human brain evolution by altering the expression of a conserved set of gene targets and provide the means to functionally link HARs with novel human brain features.