vab-21(
ju71) mutants display defects in epidermal morphogenesis and a total embryonic and larval lethality of about 50%. Examination of the embryonic development of
vab-21 mutant with time-lapse Nomarski microscopy showed that the head morphological defect and embryonic arrest occurred during embryonic elongation at two-fold and three-fold stages respectively.
vab-21(
ju71) maps to chromosome II and fails to complement maDf4 .
ju71/maDf4 heterozygotes display a higher larval lethality than
ju71 homozygotes, suggesting
ju71 is not a null allele. The phenotypes of
vab-21 mutants are rescued by a subclone that contains a single predicted gene, F10C1.2, which encodes an intermediate filament gene denoted IF-
b1 (Dodemont, et. al. EMBO J. 13: 2625-2638). This gene encodes two isoforms, differing at the N-termini due to alternative 5' exons. A 6kb genomic subclone of the shorter variant of IF-
b1 fully rescues
vab-21 mutants. We are currently determining the lesion associated with the
vab-21(
ju71) mutation. A GFP fusion transgene of VAB-21/IF-
b1 shows localization to epidermal fibrous organelles (FOs). To study the role of
vab-21 in the establishment of FOs and the coordination of the cytoskeletons in epidermal morphogenesis, we are examining the expression patterns of other components of FOs and of the epidermal cytoskeletal components in
vab-21 mutants. To ask whether
vab-21 functions redundantly with other intermediate filaments (IFs) in epidermal morphogenesis, we are currently constructing double mutants with
mua-6, which encodes another epdiermal intermediate filament protein, IF-
a2 (Hresko, et. al. 2000 Midwest worm meeting). To explore the role of
vab-21 in embryonic morphogenesis, we have constructed double mutants of
vab-21 with elongation defective mutants,
sma-1(
e30) and
vab-9(
ju7) respectively . Both double mutants display reduced embryonic lethality although they show additive morphological phenotypes. The mechanism of the suppression of embryonic lethality is under investigation.