A Caenorhabditis elegans homologue of hunchback is required for late stages of development but not early embryonic patterning.

Fay DS, Stanley HM, Han M, Wood WB.

Department of Molecular, Cellular and Developmental Biology, Howard Hughes Medical Institute, University of Colorado, Boulder 80309-347, USA.

Dev Biol 1999 Jan 15;205(2):240-53


                              We have cloned a Caenorhabditis elegans homologue of the Drosophila gap gene hunchback (hb) and have designated it hbl-1 (hunchback-like).
                              hbl-1 encodes a predicted 982-amino-acid protein, containing two putative zinc-finger domains similar to those of Drosophila Hunchback. The
                              gene is transcribed embryonically, but unlike the maternally expressed Drosophila hb, its mRNA is not detected in C. elegans oocytes. A
                              hbl-1::gfp reporter is expressed primarily in ectodermal cells during embryonic and larval development. Double-stranded RNA-interference
                              (RNAi) was used to indicate hbl-1 loss-of-function phenotypes. Progeny of hbl-1(RNAi) hermaphrodites exhibit a range of defects; the most
                              severely affected progeny arrest as partially elongated embryos or as hatching, misshapen L1 larvae. Animals that survive to adulthood exhibit
                              variably dumpy (Dpy), uncoordinated (Unc), and egg-laying defective (Egl) phenotypes, as well as defects in vulval morphology (Pvl). Abnormal
                              organization of hypodermal cells and expression of a hypodermal marker in hbl-1(RNAi) animals suggests that most of the phenotypes observed
                              could be due to improper specification of hypodermal cells. The pattern of hbl-1 expression is similar to that reported for the leech hunchback
                              homologue Lzf-2, suggesting that these proteins may have similar biological functions in diverse species with cellular embryos. Copyright 1999
                              Academic Press.