High impact information on pop-1

• pop-1 encodes an HMG box protein required for the specification of a mesoderm precursor in early C. elegans embryos [1].
• The Overinduced phenotype is suppressed by reduction of function of the genes pop-1 TCF and lin-39 Hox [2].
• Two other Wnt pathway regulators, wrm-1 and lit-1, have the same effect as pop-1 on Z1/Z4 asymmetry [3].
• Zygotic pop-1(RNAi) confirms the role of pop-1 in Z1/Z4 asymmetry and reveals additional roles of pop-1, including one in leader cell migration [3].
• Interfering with pop-1 zygotic function caused defects in the migration of the QL descendants that mimicked the defects in egl-20/Wnt mutants and blocked the expression of mab-5 [4].

Biological context of pop-1

• We find that sys-1 is haplo-insufficient for gonadogenesis defects and that sys-1 and pop-1 mutants display a strong genetic interaction in double heterozygotes [5].

Anatomical context of pop-1

• We suggest that the C. elegans endoderm is patterned by elements of the Wnt/pop-1 signalling pathway acting autonomously within the E lineage [6].
• I have used a novel RNA-mediated interference technique to interfere specifically with pop-1 zygotic function and have determined that pop-1 is required for wild-type T cell polarity [4].

Other interactions of pop-1

• Therefore, sys-1 is a dose-sensitive locus and may function together with pop-1 to control Z1/Z4 asymmetry [5].
• As in pop-1 mutants, dsh-2 hermaphrodites have Z1 and Z4 lineage defects indicative of defective PD polarity and are missing gonadal arms [7].

References