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BEGIN:VEVENT
DTSTAMP:20260503T212114Z
DTSTART;VALUE=DATE-TIME:20250611T131500
DTEND;VALUE=DATE-TIME:20250611T141500
SUMMARY:BMS Seminar: Transcriptional and Post-Transcriptional Regulation 
 Meet to Drive Human Evolution\, Professor Miles Wilkinson\, University o
 f California - San Diego\, USA.
TZID:Europe/London
UID:20250611-8ac672c59686280d019686726fd8013b@warwick.ac.uk
CREATED:20250430T112608Z
DESCRIPTION:Abstract: A fundamental question in biology is: how did human
 s acquire their unique characteristics? What allows us to stand upright\
 , while our primate ancestors walked on all fours? What brain alteration
 s drove our increased intelligence and allowed us to perceive our own mo
 rtality? One of the mechanisms that has been hypothesized to be involved
  is changes in gene expression elicited by nucleotide alterations in non
 -coding regions of the human genome. In my talk\, I will focus on a clas
 s of DNA sequences hypothesized to have this role. These human accelerat
 ed regions (HARs) are segments of DNA that exhibit 3 characteristics tha
 t—together—make them prime candidates for specifying human-specific trai
 ts by altering patterns of gene expression. First\, HARs have rapidly ch
 anged in sequence specifically in the human lineage. Second\, HARs are h
 ighly conserved in sequence in all mammals or vertebrates\, indicating t
 hey that must have been selected for the ability to confer one or more f
 unction in higher organisms. Third\, the vast majority of HARs are in th
 e non-coding portion of animal genomes\, indicating that most are likely
  to have a regulatory function. While HARs are hypothesized to confer hu
 man-specific traits\, this has yet to be demonstrated. In my talk\, I wi
 ll describe a HAR—called “HAR123”—that has properties consistent with su
 ch a role in the nervous system. We elected to focus on HAR123 because i
 t is in the intron of a gene essential for a RNA turnover pathway—nonsen
 se-mediated RNA decay (NMD)—that has roles in the nervous system and who
 se disruption causes neural disease. Through both in vitro and in vivo s
 tudies\, we discovered that HAR123 is a conserved transcriptional enhanc
 er that influences nervous system development and function. HAR123 promo
 tes human neural progenitor cell (NPC) formation\, influences the ratio 
 of neurons and glial cells produced from NPCs\, and functions in cogniti
 ve flexibility in vivo. We identified targets of HAR123 and found that o
 ne of these targets\, HIC1\, acts downstream of HAR123 to promote NPC ge
 neration. We also obtained evidence that HAR123 upregulates the expressi
 on of SMG6 in specific brain regions\, raising the possibility that HAR1
 23 evolved in the human lineage to regulate RNA turnover in a brain regi
 on-specific manner. Finally\, we found that the human and chimpanzee ort
 hologs of HAR123 subtly differ in their molecular and cellular effects\,
  consistent with the possibility that HAR123 has evolved since the human
 -chimpanzee split to influence nervous system traits specific to humans.
 
LOCATION:IBRB Lecture Theatre
CATEGORIES:BiomedicalSciences,Directorate Seminars
LAST-MODIFIED:20250430T112608Z
ORGANIZER;CN=Jas Bains:
END:VEVENT
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