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#Notch signaling

11 public questions tagged with this topic.

Elegans -ll

What happens in embryos lacking functional LAG-2?

LAG-2 encodes Delta-like ligand for LIN-12 and GLP-1 Notch receptors. In early embryo, ABa and MS express GLP-1 while P2 presents LAG-2 and APX-1 to activate GLP-1 in ABp for A-P patterning of pharynx. In gonad, Z1.ppp/Z4.aaa require LAG-2/LIN-12 interaction to decide anchor cell versus ventral uterine fate. Without functional LAG-2, GLP-1 and LIN-12 receptors remain unbound, NICD cleavage fails, downstream targets lag-1 dependent transcription silent. Consequently ABp to ABa transformation and AC/VU defects occur, but fundamentally LIN-12 remains inactive due to absent ligand triggering, revealing ligand-dependent activation mode of Notch signaling in nematode.

Ref: Henderson et al. 1994; Gilbert Chapter 4: LAG-2 loss - LIN-12 remains inactive due to ligand absence.

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Elegans -ll

What happens in embryos with a constitutively active LIN-12 receptor?

Constitutively active LIN-12 results from gain-of-function mutation deleting extracellular domain, making receptor ligand-independent. Normally LIN-12 Notch restricts primary fate via lateral signaling, promoting secondary fate in P5.p and P7.p. When all VPCs express activated LIN-12, Ras-MAPK mediated primary program blocked by LIN-12 targets lip-1 phosphatase that dephosphorylates MAPK, and lst inhibitors. Consequently even P6.p high LIN-3 cannot sustain primary, all P3.p-P8.p express secondary vulval markers and generate secondary lineages producing symmetrical vulval structures without central primary invagination. This phenotype parallels LIN-12 dominant mutants described by Greenwald showing all secondary fate adoption.

Ref: Greenwald et al. 1983; Gilbert Chapter 15: Constitutively active LIN-12 - all VPCs become secondary.

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Elegans -ll

Which of the following correctly describes the effect of glp-1 mutation in C. elegans embryos?

GLP-1 encodes C. elegans Notch receptor essential for AB lineage distinction. After first cleavage, P2 Delta signals via APX-1/LAG-2 activate GLP-1 only in ABp because ABa contact with P2 is minimal. This induces ABp-specific gene expression, including repression of LAG-2 in ABa. In glp-1 loss-of-function embryos, Notch signaling absent in ABp, so ABp defaults to ABa program, producing two ABa-like lineages with duplicated anterior pharynx cells and loss of dorsal ventral patterning. EMS division unaffected but overall embryo fails pharyngeal asymmetry. Thus transformation is ABp to ABa, classic Notch lineage conversion evidence.

Ref: Priess 2005; Gilbert, Developmental Biology 12th ed., Chapter 4: glp-1 mutation - ABp transforms into ABa.

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Cell Signaling Dev Bio & Other Pathways

Matrix metalloprotease involved in Notch signaling is

ADAM10, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling Dev Bio & Other Pathways

DSL proteins refer to

Delta, Serrate, Lag-2, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling Dev Bio & Other Pathways

NICD translocates to nucleus and binds with

CSL/RBPJ, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling Dev Bio & Other Pathways

γ-secretase cleaves Notch to release

Notch intracellular domain, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling Dev Bio & Other Pathways

ADAM10 cleaves Notch at which stage?

After Delta binding at cell surface, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling Dev Bio & Other Pathways

Initial proteolytic cleavage of Notch in Golgi is mediated by

Furin protease, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling Dev Bio & Other Pathways

The ligand Delta is expressed on which cell?

Signaling cell, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling ELR Pathways - I

Notch signaling involves

proteolytic cleavage of receptor, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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