Hox paper exam 1.txt

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rincrocci
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Hox paper exam 1.txt
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2013-10-07 00:25:54
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hox
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  1. Lovegrove Hox gene article
  2. Hox gene roles:
    • A TF that leads to body segregation, by directing morphogenesis of SEGMENT specific STRUCTURES
    • Targets of Hox genes are TFs and signaling molecules, resulting in the expression of REALIZATOR genes.
    • These realizators are involved with:
    • 1. cell adhesion
    • 2. cell polarity
    • 3. cytoskeleton regulation
    • Look at Hox gene Abdominal-B in the paper
  3. Fig 1: Looking at posterior spiracle formation
    • See the spiracle formation and the trachea with Hox genes
    • With Hox genes removed (Abd-B), posterior spiracle missing
    • WIth mutants (dom, ct, sal, ems) downstream of Abd-B, spiracle defects still seen
  4. CELL POLARITY Fig 2: Apico-Basal cell polarity markers show that Abd-B induced spiracle gene cascade is involved with CELL POLARITY gene Transcription
    • Cell polarity markers used:
    • Sas showed that it forms in the spiracular chamber cells in the apical membranes
    • E-Cad, Dlg, Nrt showed similar results, expanded in the apico-basal membrane domains
    • Ectopic Abd-B activation showed similar cell polarity in ectopic regions where spiracle formation occurred
  5. CELL POLARITY CONT Fig 3: Posterior spiracle expression with Crumb, regulated by JAK/STAT pathway
    • Crumb(crb) is seen upregulated in spiracle cells, but when the JAK/STAT ligand is missing, there is loss of crb expression (looked at via reporter system
    • When crb mutants, the spiracles are all shortened.
    • However crb cannot rescue the JAK/STAT loss of fxn phenotype, so crb must be coregulated during spiracle elongation by JAK/STAT
  6. CELL ADHESION Fig 4: Non-classical E-cadherins (4 shown) activate in spiracle cells require Abd-B function
    • Expression of e-cads in WT spiracle cells and in Abd-B mutants showed they all stopped expression
    • With mutants of downstream targets to Abd-B (sal, ct, ems) showed lack of expression also
    • upd (no Ligand) shows some JAK/STAT pathway activation is needed
  7. CELL ADHESION Fig 5: Nonclassical cadherins interact with E-cad
    • Cad74A tagged w/GFP showed that it is at the adherin junctions next to B-catenin
    • E-cadherin mutants FAIL to invaginate spiracle cells AND cause spiracle defects when non-classical Cadherins are REDUCED
  8. CYTOSKELETON Fig 6: Rho GTPases in posterior spiracle depend on Abd-B
    • in Hox mutant Abd-B, the cv-c (GTPase activating gene) is REDUCED
    • in ectopic Abd-B, higher levels of cv-c are seen
    • GTPase exchange factor Gef64c: showed reduction in Abd-B mutants and in JAK/STAT ligand missing (upd) cells, as well as loss with ems downstream mutant

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