You are examining blood vessel malformations in a mouse disease model. You decide to isolate vascular endothelial cells to watch how they grow in culture. You notice that the blood vessels show excessive sprouting and tip cell formation. You suspect the mutant cells may have a mutation in the Notch1 receptor as stimulating the receptor with ligand does not reduce the extent of sprouting, suggesting Notch1 signaling is defective in these cells. How might the mutation affect Notch1 signaling activity? The mutation may affect cleavage of the c-terminus of Notch1 and translocation to the nucleus The mutation may affect the ability of Notch1 to activate cytoplasmic DII4 The mutation may affect the ability of Notch1 to self-dimerize at the membrane The mutation may affect the ability of Notch1 to activate itself via phosphorylation of the c-terminal portion of the receptor
Added by Donald K.
Close
Step 1
This suggests that there is a defect in Notch1 signaling activity in these cells. Show more…
Show all steps
Your feedback will help us improve your experience
Sri K and 98 other Biology educators are ready to help you.
Ask a new question
Labs
Want to see this concept in action?
Explore this concept interactively to see how it behaves as you change inputs.
Key Concepts
Recommended Videos
You have developed a unique hypothetical mouse fibroblast cell in culture. In that context, using the CRISPR-Cas9 gene-editing technology, you have mutated the Sos protein of the receptor tyrosine kinase pathway by replacing all the prolines of the Sos. As a result of the created mutations, the Sos can still bind to the SH3 domain of the GRB2 but has lost the binding ability to Ras. Now, you have treated the cells with FGF (fibroblast growth factor), which signals through the receptor tyrosine kinase pathway. Surprisingly, you see that the growth and division of the fibroblasts are arrested. Which of the following mechanisms explains your observation? (B) The Ras will remain in the GDP-bound inactive state and prevent downstream factors required for signaling to turn on transcription for cell division and growth. (C) The receptor tyrosine kinase will not dimerize after the event of adding FGF and will stop any further signaling. (A) The Ras will not be able to hydrolyze GTP. Both B and C are correct.
Sri K.
Madhur L.
Two spontaneous IgA deficiency mutations, named noa-1 and noa-2, arose independently in different mice of the same inbred strain. Both mutations segregate as single autosomal traits, and do not involve the MHC. To investigate the nature of these mutations, you perform the following experiment. You isolate CD4+ T cells from each strain, activate them in vitro, and collect supernates. You next isolate mature splenic B cells from each strain and stimulate them in vitro with the various T cell supernates. After three days, you use ELISA to measure IgM and IgA production, and PCR analyses to assess switch recombination events into the alpha heavy chain switch regions. [N.B.: All B cell cultures made some IgM and IgG] Table 1: IgA production and s-Ě‘ rearrangements in cultures of B cells and T cell supernates from normal and IgA deficient mice B cell source: wt, noa-1, noa-2 T cell sup source: wt, noa-1, noa-2 (for each B cell source) IgA production: wt B cell: + (wt), - (noa-1), + (noa-2) noa-1 B cell: + (wt), - (noa-1), + (noa-2) noa-2 B cell: - (wt), - (noa-1), - (noa-2) switch-Ě‘ rearrangements: wt B cell: + (wt), - (noa-1), + (noa-2) noa-1 B cell: + (wt), - (noa-1), + (noa-2) noa-2 B cell: + (wt), - (noa-1), + (noa-2) Advance a hypothesis regarding the nature of the mutation(s).
Recommended Textbooks
Biology for AP Courses
Objective Biology for NEET
Introduction to General, Organic and Biochemistry
Transcript
18,000,000+
Students on Numerade
Trusted by students at 8,000+ universities
Watch the video solution with this free unlock.
EMAIL
PASSWORD