C-Elegans Development-l

C-Elegans Development-l

Which phenotype results from a loss-of-function mutation in SKN-1?

SKN-1 specifies mesendodermal progenitors central to nematode gastrulation and gut formation. Maternal SKN-1 accumulates in EMS nucleus where it directly binds promoters of med-1,2 GATA factors, which activate end-1,3 and tbx-35 to segregate endoderm versus mesoderm lineages differentially. Null skn-1 alleles lack pharynx derived from MS, body wall muscle from MS, intestine derived from E, causing embryonic lethality with excess skin, neurons but no gut markers. Rescue shows autonomous requirement in EMS not P2. Thus loss mirrors mesendoderm deletion rather than vulval defects highlighting master regulator role.

Ref: Bowerman et al., Cell 1992: SKN-1 mutants lack mesoderm and endoderm derivatives from EMS lineage.

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C-Elegans Development-l

What is the role of PAR proteins in early C. elegans development?

PAR family establishes early embryonic polarity without zygotic transcription relying solely on maternal proteins and sperm cue. PAR-2 RING finger protein recruited posteriorly after sperm centrosome signal suppresses anterior actomyosin contractility via RhoGAP regulation, preventing PAR-3/PAR-6/PKC-3 complex binding posteriorly. PAR-3 scaffolds anterior complex regulating cortical contractility and spindle positioning via GPR-1/2 and LIN-5. Mutual antagonism creates bistable cortical domains translated into cytoplasmic gradients MEX-5 anterior high and PIE-1 posterior high via differential phosphorylation. Conservation from worms to mammals underscores fundamental cortical polarity principle defining axes before gastrulation.

Ref: Kemphues, Annual Review Cell Dev Biology: PAR proteins localize to cortex establishing anterior-posterior polarity.

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C-Elegans Development-l

Which signaling pathway regulates EMS cell fate in response to P2 signaling?

EMS fate specification integrates Wnt signaling from neighbor P2 historically termed Wnt/MAPK or Wnt/beta-catenin asymmetry pathway. MOM-2 Wnt produced by P2 signals via MOM-5 Frizzled, MOM-4 TAK1 MAPKKK, WRM-1 beta-catenin, LIT-1 Nemo-like kinase to EMS, activating MAPK-like cascade depleting nuclear POP-1 TCF from posterior daughter E via phosphorylation-triggered export. Low POP-1 converts from repressor to activator enabling END-1,3 expression and gut differentiation. Notch pathway distinguishes AB fate, but EMS specification relies primarily on Wnt asymmetry. Genetic removal of mom genes converts E to MS.

Ref: Rocheleau et al., Cell 1997: Wnt signaling via WRM-1 and LIT-1 regulates EMS fate in response to P2.

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C-Elegans Development-l

Which of the following is required for nuclear migration during C. elegans fertilization?

During fertilization, maternal and paternal pronuclei must migrate centrally and meet before first mitosis for syngamy and diploidy. Sperm aster nucleated by centriole centrosome extends astral microtubules interacting with cortex. Dynein heavy chain DHC-1 with dynactin DNC-1, adaptor LIS-1, and nuclear envelope bridge SUN-1/ZYG-12 KASH drives minus-end directed pulling forces anchored at cortex. Cytoplasmic dynein reels pronuclei inward while pushing female pronucleus posteriorly. Kinesin KLP-18 opposes but dynein dominates net movement. Dynein inhibition via RNAi causes pronuclei to remain peripheral and asymmetric division failure.

Ref: Gonczy et al., Journal Cell Biology: Dynein-driven pronuclear migration and centrosome positioning in C. elegans zygote.

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C-Elegans Development-l

Which protein prevents somatic differentiation in germline cells?

PIE-1 contains tandem CCCH zinc fingers highly enriched in P lineage P2-P4 and germline precursors associated with P-granules. It binds and inhibits P-TEFb cyclin T CDK-9 transcription elongation factor, blocking Ser2 phosphorylation of RNA polymerase II carboxy-terminal domain globally repressing mRNA synthesis. This prevents activation of somatic genes hlh-1 muscle, pha-4 pharynx, elt-2 intestine normally induced by SKN-1 and PAL-1. PIE-1 colocalizes with P-granules protecting germline genome via small RNA pathways including PRG-1. Mutants lacking PIE-1 show P2 transforming into EMS-like cells producing gut at expense of germline.

Ref: Mello et al., Science 1996: PIE-1 zinc-finger protein prevents somatic differentiation in germline by repressing transcription.

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C-Elegans Development-l

What happens in embryos lacking PAL-1 function?

PAL-1 is Caudal-like homeodomain transcription factor maternally deposited posteriorly via post-transcriptional control by MEX-3 RNA-binding protein, MEX-5/6 and SPN-4 regulating translation efficiency. It activates posterior program genes including tbx-8/9 T-box and elt-3 in EMS descendants C and D blastomeres producing body wall muscle, hypodermis, intestine-associated muscle. C blastomere generates hypodermis and muscle, D generates muscle only. In pal-1 mutants or RNAi knockdown, posterior blastomeres transform to anterior-like EMS fates, lacking muscle myosin MYO-3 and COL cuticle markers, causing embryonic arrest with absent C and D lineages.

Ref: Hunter & Kenyon, Cell 1996: PAL-1 Caudal homolog required for C and D blastomere specification.

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C-Elegans Development-l

Which protein prevents LIN-3 signaling in tertiary vulval precursor cells?

Tertiary vulval precursor cells must avoid responding to low LIN-3 despite molecular competence maintained by LIN-39. LIN-12 Notch activity in P3.p, P4.p, P8.p and induced cells modulates EGFR sensitivity by cross-inhibition. LIN-12 signaling upregulates LIP-1 dual-specificity MAPK phosphatase, LST-1-4 inhibitors, DPY-23 adaptin dampening LET-23/MAPK cascade and Ras output. Additionally, LIN-12 promotes expression of synMuv B genes including lin-35 retinoblastoma antagonizing EGF induction via chromatin remodeling. This reciprocal inhibition between RTK and Notch ensures only P6.p attains high MAPK, distal VPCs remain hypodermal despite low LIN-3.

Ref: Sternberg, WormBook Vulval development: LIN-12 Notch inhibits MAPK via LIP-1 and lst to block tertiary response.

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C-Elegans Development-l

Which of the following determines the dorsal-ventral axis in C. elegans?

Dorsal-ventral axis in C. elegans originates from early cell contacts rather than diffusible gradients like BMP in vertebrates. At four-cell embryo, AB and P1 touching geometry differentially positions ABp contacting P2 receiving GLP-1 Notch signal involving APX-1, while ABa does not contact P2. This differential contact plus SKN-1, PAR polarity cues orients mitotic spindles via GPR-1/2 G-alpha regulation, positioning descendants dorsally versus ventrally. Physical interaction between AB derivatives and P1 lineage mediated by cadherin HMR-1 and catenin HMP-1 translates contact asymmetry into fate segregation essential for nervous system positioning.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: AB-P1 interaction establishes dorsal-ventral axis via Notch.

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C-Elegans Development-l

Which protein is the C. elegans homolog of Delta, involved in lateral inhibition?

Delta-Notch lateral signaling components are conserved across nematodes, flies, vertebrates. LAG-2 encodes transmembrane DSL ligand homologous to Drosophila Delta with multiple EGF repeats and DSL domain required for Notch binding, expressed in anchor cell and P2 signaling cells. Its extracellular domain binds LIN-12 and GLP-1 Notch receptors triggering metalloprotease S2 and presenilin gamma-secretase S3 cleavage, releasing NICD transcription complex with LAG-1 CSL and SEL-8 Mastermind activating hes homologs. LAG-2 patterning ensures single anchor cell and ABp induction, making canonical Delta equivalent mediating juxtacrine communication.

Ref: Tax et al., Nature 1994: LAG-2 is Delta homolog, ligand for LIN-12 and GLP-1 Notch receptors.

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C-Elegans Development-l

Which of the following mutations leads to a Multivulva (Muv) phenotype?

LIN-12 encodes Notch family transmembrane receptor regulating temporal, somatic gonad, and vulval fates through lateral signaling feedback. Gain-of-function alleles cause constitutive Notch intracellular domain signaling independent of LAG-2 ligand due to missense in extracellular EGF repeats or intracellular PEST degradation domain. In VPCs, ectopic LIN-12 drives excessive secondary fate adoption, antagonizing MAPK primary induction feedback leading to multiple ventral invaginations or multivulva phenotype with extra pseudovulvae expressing 2° markers. Conversely, loss yields two anchor cells, demonstrating dosage sensitivity of Notch balancing 1° versus 2° outcomes.

Ref: Sternberg, WormBook Vulval development: Gain-of-function LIN-12 causes multivulva via ectopic secondary fate induction.

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C-Elegans Development-l

Which protein localizes to the posterior pole of the C. elegans zygote?

PAR-1 is serine-threonine kinase homologous to mammalian MARK2 microtubule affinity-regulating kinase, localizing to posterior cortex soon after fertilization following sperm-derived centrosome cue. Centrosome reduces anterior NMY-2 actomyosin contractility, allowing PAR-2 RING finger to recruit PAR-1 to posterior membrane via lipid binding. PAR-1 phosphorylates MEX-5, MEX-6 and PAR-3 at conserved serines to maintain anterior restriction, creating bistable cortical domains. Posterior enrichment ensures P-granule retention, proper spindle rotation via GPR-1/2, size asymmetry, germline segregation, and embryonic viability essential for polarity maintenance and lineage fidelity throughout early development.

Ref: Goldstein & Macara, Nature Cell Biology: PAR-1 posterior kinase establishing embryonic polarity and P-granule localization.

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C-Elegans Development-l

Which of the following describes the fate of P3.p, P4.p, and P8.p in normal development?

Vulval precursor equivalence group spans P3.p-P8.p in ventral hypodermis, maintained by LIN-39 Hox preventing hypodermal fusion during larval stages. In wild type, only P5.p-P7.p receive sufficient LIN-3 EGF from anchor cell during L3 stage to induce vulval fates via Ras-MAPK and BAR-1 Wnt competence. P3.p, P4.p, P8.p receive below-threshold LIN-3 due to distance and are uninduced, adopting tertiary 3° fate, fusing with hyp7 syncytium via EFF-1 fusogen without dividing, becoming part of large hypodermal syncytium, not contributing to vulva, representing default epidermal fate when RTK absent.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: Fate of uninduced VPCs - fusion with hyp7 and tertiary fate.

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