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Please use this identifier to cite or link to this item: http://arks.princeton.edu/ark:/88435/dsp01ks65hg54c
Title: Investigating the Role of Prdm1 in the Heart Development of Ciona intestinalis
Authors: Kim, Haram
Advisors: Levine, Michael
Department: Molecular Biology
Class Year: 2024
Abstract: Ciona intestinalis is an ascidian species that shares genetic and anatomical homologies with vertebrates, one of which being the Prdm gene, which has multiple functions including a key role in the development of the nervous system. In humans, Prdm1 has been implicated in tumor suppression, immune cell differentiation, and the formation of the aorta. Two Prdm1 paralogs, Prdm1-r.a/b, are expressed during embryogenesis of Ciona, and are downstream targets of the FGF signaling pathway, activated by ERF derepression. Recent findings have shown unexpected Prdm1-r.a/b expression in the B7.5 cells, which give rise to heart precursor cells. Despite previous studies on Prdm1 in the Ciona nervous system, its specific regulatory mechanisms and functions in the heart precursor cells remain unclear. This study sought to establish the relationship between Prdm1 and other potential upstream and downstream targets. Through spatiotemporal in-situ analysis, a precise onset of genes involved in the specification of the B7.5 cells was determined, suggesting that the specification of the heart precursor cells is more complicated than previously assumed. Reporter assays identified potential enhancers for Prdm1-r.a/b immediately upstream of their promotors. Furthermore, overexpression of Prdm1-r.a led to increased proliferation of B7.5 cells and reduced the expression of CDKN1B, a mitosis inhibitor, suggesting the role of Prdm1 as a repressor of CDKN1B. This work highlights the regulatory role of Prdm1-r.a/b in Ciona heart development by ensuring the appropriate number of precursor cells during embryonic stages.
URI: http://arks.princeton.edu/ark:/88435/dsp01ks65hg54c
Type of Material: Princeton University Senior Theses
Language: en
Appears in Collections:Molecular Biology, 1954-2024

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