rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    non sort: A
    title: RAP2>CNH-MAP4K Signaling Pathway Promotes Non-Specialized Epithelial Cell Fate in So-Called Ground/Passive/Uninduced Cells
  name:
    name part: Fakieh, Razan A.
    role:
      role term: creator
    role:
      role term: author.
  name:
    name part: Reiner, David
    role:
      role term: thesis advisor.
  name:
    name part: Texas A&M University
    role:
      role term: degree granting institution.
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2023
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: remote
    extent: 1 online resource.
  abstract: During C. elegans development, EGF signal from the anchor cell (AC) induces the roughly six equipotent vulval precursor cells (VPCs) to assume the pattern 3˚-3˚-2˚-1˚-2˚-3˚ of cell fates. The VPC closest to the AC is induced via the Ras-Raf-MEK-ERK MAP kinase cascade to assume 1˚ fate. Presumptive 1˚ cells express DSL ligands to induce the two neighboring cells via the Notch receptor to assume 2˚ fate. In contrast, 3˚ fate is typically referred to as the "ground" or "uninduced" cell fate; 3˚ cells divide once and fuse with the surrounding epithelium. We observed that MIG-15, a MAP4 kinase, plays a role in VPC patterning. Upon genetic perturbation of MIG-15 function, we observed an increase in ectopic 1˚ as well as ectopic 2˚ cells. This is also true for RAP-2, a protein shown in various systems to activate MIG-15. Both RAP-2 and MIG-15 are necessary for full expression of a marker expressed in 3° cells. Endogenous CRISPR tags of MIG-15 and RAP-2 revealed ubiquitous expression with cytosolic and cell-membrane localization of both genes respectively. Our work positions us to explore signals that promote "ground" developmental state and perhaps informs the relationship between cancers and stromal cells. The electronic version of this dissertation is accessible from https://hdl.handle.net/1969.1/198706
  note: by Razan Fakieh.
  note: "Major Subject: Medical Sciences"
  note: Includes vita.
  note: Doctor of Philosophy Texas A&M University 2022 https://hdl.handle.net/1969.1/198706
  note: Includes bibliographical references.
  note: Text (Dissertation)
  subject:
    topic: Major Medical Sciences
  subject:
    topic: Cell fate
  subject:
    topic: Developmental biology
  subject:
    topic: C.elegans
  subject:
    topic: cell signaling
  subject:
    topic: CRISPR
  identifier: https://hdl.handle.net/1969.1/198706
  record info:
    record content source: TXA
    record creation date: 250130
    record change date: 20250326141437.1
    record identifier: in00005621421
    language of cataloging:
      language term: eng