Elegans -ll

Elegans -ll

Which protein is essential for E cell fate in C. elegans?

E cell, posterior daughter of EMS, requires combinatorial inputs from SKN-1, MED-1/2 and Wnt-modified POP-1 to activate end-1 and end-3 GATA factors specifying intestine. Maternal SKN-1 activates med genes broadly in EMS lineage; Wnt signal from P2 causes reduction of POP-1 in E, converting it from repressor to coactivator with SYS-1 beta-catenin. Modified POP-1 together with SKN-1 induced MEDs binds endoderm enhancers, driving END-1/3 expression. POP-1 null causes both EMS daughters to become E-like, revealing essential role in distinguishing MS versus E. Hence POP-1 essential for activating E fate in cooperation with Wnt signaling pathway.

Ref: Maduro et al. 2005; Gilbert Chapter 4: POP-1 essential for E cell fate specification in C. elegans endoderm.

View Details

Elegans -ll

What determines the default fate of EMS blastomere?

EMS blastomere default state without P2 signal is mesodermal MS fate. This is determined by nuclear POP-1 levels. In anterior MS daughter, high nuclear POP-1 binds and represses end-1 promoter together with histone deacetylases, allowing tbx-35 for pharynx and muscle. Low POP-1 permits endoderm. POP-1 repression defines default program: when Wnt signaling absent, both daughters maintain high POP-1 and become MS-like. SKN-1 provides competence for both MS and E, but fate choice gated by POP-1 differential. Therefore POP-1 concentration acts as binary switch establishing MS as ground state, repressed variant requiring Wnt input for E divergence.

Ref: Lin et al. 1995; Gilbert Chapter 4: POP-1 determines default fate of EMS blastomere as MS.

View Details

Elegans -ll

Which factor ensures ABp fate specification?

ABp fate distinguishing dorsal versus ventral AB lineage derivatives depends on GLP-1 Notch receptor activation. GLP-1 protein segregates to all AB daughters but functionally active only in ABp due to contact with P2 ligands APX-1 and LAG-2. Activated GLP-1 ICD upregulates Notch target genes ref-1 family, promoting ABp-specific blastomere divisions generating dorsal epidermis and distinct pharyngeal cells. In glp-1 mutants ABp transforms to ABa, equalizing lineage. Therefore GLP-1 presence and selective activation is decisive intrinsic factor ensuring ABp identity, integrating positional signal from P2 to create anterior-posterior and dorsal-ventral pattern within early embryo ectoderm contribution.

Ref: Mango et al. 1994; Gilbert Chapter 4: GLP-1 Notch receptor ensures ABp fate specification in C. elegans.

View Details

Elegans -ll

What happens when three central vulval precursor cells are ablated?

Vulval precursor cells demonstrate regulative ability. Normally P5.p-P7.p generate vulva, but if three central VPCs ablated by laser during early L3 before induction, neighboring P3.p, P4.p or P8.p which would normally fuse to hyp7 can be recruited. They possess latent competence sustained by LIN-39 and Wnt signals, and when anchor cell LIN-3 gradient shifts to them, activate LET-23 Ras-MAPK cascade converting to vulval fates, forming functional though sometimes reduced vulva. This regulative compensation illustrates conditional specification within equivalence group, where cell-cell interactions compensate for loss, ensuring robustness of organogenesis despite perturbations during larval development.

Ref: Sternberg & Horvitz 1986; Gilbert Chapter 15: Remaining cells compensate after central VPC ablation and form vulva.

View Details

Elegans -ll

Which of the following mutations leads to excess uterine tissue formation?

LIN-12 Notch controls binary decision between anchor cell and ventral uterine precursor within gonad. During L2 stage, Z1.ppp and Z4.aaa express both LAG-2 ligand and LIN-12 receptor. Lateral interaction amplifies slight difference so cell with higher LIN-12 becomes ventral uterine precursor continuing division, while other with lower LIN-12 becomes anchor cell. Gain-of-function lin-12 mutants with constitutively active NICD cause both Z1.ppp and Z4.aaa to adopt ventral uterine fate, producing two ventral uteri, loss of anchor cell, extra uterine tissue and failure to induce vulva. Thus excess LIN-12 activity leads to duplication of uterine lineage at expense of AC.

Ref: Greenwald et al. 1983; Sternberg Vulval Chapter: Gain-of-function lin-12 leads to excess uterine tissue formation.

View Details

Elegans -ll

Which of the following describes the function of LAG-2?

LAG-2 is C. elegans Delta/Serrate/Lag2 family ligand for Notch receptors LIN-12 and GLP-1. Expressed in P2, anchor cell and primary VPC P6.p, LAG-2 extracellular DSL domain binds Notch extracellular EGF repeats triggering two proteolytic cleavages by ADAM and gamma-secretase, releasing Notch intracellular domain that complexes with LAG-1 to activate transcription. In AB lineage, LAG-2 from P2 activates GLP-1 to specify ABp fate; in vulva, LAG-2 from P6.p activates LIN-12 to specify secondary fates. Therefore general biochemical description is Notch ligand, essential for lateral and inductive Notch signaling in multiple cell fate decisions during early embryogenesis.

Ref: Henderson et al. 1994; Gilbert Chapter 4: LAG-2 functions as Notch ligand for GLP-1 and LIN-12.

View Details

Elegans -ll

What is the function of MOM-2 in C. elegans?

MOM-2 encodes C. elegans Wnt homolog expressed in P2 blastomere at 4-cell stage. It binds MOM-5 Frizzled receptor on EMS, collaborating with MES-1/SRC-1 pathway to activate WRM-1 beta-catenin and MAPK signaling, resulting in phosphorylation and downregulation of POP-1 TCF in posterior daughter E. Converted POP-1 together with higher SYS-1 beta-catenin activates transcription of end-1, end-3 endoderm determinants. mom-2 mutants phenocopy loss of P2 signal, causing both EMS daughters to become MS-like. Thus primary function of MOM-2 is to activate Wnt signaling establishing EMS polarity and endoderm specification.

Ref: Thorpe et al. 1997; Gilbert Chapter 4: MOM-2 function - activates Wnt signaling in EMS specification.

View Details

Elegans -ll

Which of the following occurs in skn-1 mutant embryos?

SKN-1 is maternally deposited transcription factor required for EMS blastomere descendant fates. In skn-1 null or strong loss-of-function embryos generated by RNAi, transcriptional activation of med-1, med-2 fails, so cascade leading to end-1, end-3, tbx-35, ceh-51 not induced. EMS produces daughters that do not form pharynx mesoderm from MS or intestine from E, instead adopts C-like muscle fate producing excess body wall muscle, while overall embryo arrests. Hence loss of EMS-derived lineages including intestinal, pharyngeal and body wall muscle subsets normally sourced from MS and E leads to failure of gut formation and embryonic lethality with phenotype lacking endoderm.

Ref: Bowerman et al. 1993; Gilbert Chapter 4: skn-1 mutant embryos loss of EMS-derived lineages.

View Details

Elegans -ll

Which pathway regulates left-right asymmetry in C. elegans?

Left-right asymmetry in C. elegans morphogenesis involves Nodal-related signaling despite absence of classical Nodal in worms. Recent work identifies UNC-6/Netrin and TGFbeta family member TIG-3 related to Activin/Nodal acting through SMA-6 and DAF-4 receptors regulating asymmetric positioning of gut, gonad and AB lineage divisions such as ABar spindle skewing. While early cleavage asymmetry uses Notch and Wnt, later organ laterality requires this Activin-like cascade. Although vertebrates use Nodal-Lefty-Pitx2, conserved type I and II TGFbeta pathway components were shown to influence nematode left-right handedness of blastomere divisions and gut rotation, classified as Nodal/Activin related signaling module.

Ref: WormBook Embryogenesis: Nodal/Activin-related pathway regulates left-right asymmetry in C. elegans embryogenesis.

View Details

Elegans -ll

Which motor protein is responsible for P-granule migration?

P-granules, ribonucleoprotein assemblies marking germline, segregate to posterior blastomere P1 during first division and subsequently to germline precursors P2-P4. Their posterior migration along cell cortex before division requires microtubule motor dynein transporting granule components along cortical microtubules toward centrosome at posterior pole. PAR-1 dependent microtubule organization creates flow. Mutants in dynein heavy chain dhc-1 or its regulator dynactin cause equal distribution of P-granules to both AB and P1, losing germline restriction. Myosin II and kinesin contribute to cortical flows but dynein-driven transport is primary driver ensuring germ plasm inheritance by germline lineage.

Ref: Updike & Strome 2010; Gilbert Chapter 4: Dynein motor responsible for P-granule migration in early embryo.

View Details

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.

View Details

Elegans -ll

Which protein prevents LIN-3 activation in tertiary VPCs?

Lateral inhibition ensures tertiary fate protection. After induction, P6.p primary cell expresses LAG-2 ligands activating LIN-12 Notch in P5.p and P7.p, specifying secondary fate. Secondary cells also secrete DSL signals that activate LIN-12 in more distant P3.p, P4.p, P8.p. LIN-12 activation induces transcriptional repressors that prevent activation of LET-23 EGFR pathway by low LIN-3 and promotes hyp7 fusion via inhibition of egl-17 and vulval genes. Thus LIN-12 prevents LIN-3 activation from specifying vulval fate in tertiary cells, ensuring correct 3-2-1-2-3 pattern by restricting EGFR responsiveness through Notch-mediated lateral inhibition mechanism.

Ref: Sternberg WormBook Vulval Development: LIN-12 prevents LIN-3 activation in tertiary VPCs via lateral inhibition.

View Details