High impact information on hkb

• We identified a new allele of hairy in a mutagenesis screen and showed that hairy mutations cause branching and bulging of the normally unbranched salivary tube, in part through prolonged expression of huckebein (hkb) [1].
• Repression does not require either tailless or huckebein, which were previously thought to constitute the sole zygotic output of the tor signaling system [2].
• Thus, hkb is necessary for endoderm development and its activity defines spatial limits within the blastoderm embryo in which the germ layers are established [3].
• Conversely, ectopic expression of hkb inhibits the formation of the major gastrulation fold which gives rise to the mesoderm and prevents normal segmentation in the ectoderm [3].
• Trg is expressed throughout embryogenesis, first at the blastoderm stage in the hindgut primordium under the control of the terminal gap genes tll and hkb, and then until the end of embryogenesis in the differentiating hindgut [4].

Biological context of hkb

• In the absence of terminal gap gene activities, as in hkb and tll mutant embryos, the expression domains of the central gap genes expand posteriorly, indicating that the terminal gap gene activities prevent central gap gene expression in the posterior pole region of the wildtype embryo [5].
• Like NB 7-3, the progenitor(s) of these ectopic cells express Huckebein (Hkb), another zinc finger protein [6].
• We examined the interplay between DI, Gro and Dri on the hkb enhancer and show that when acting over a distance, Gro abolishes rather than converts DI activator function [7].
• Integration of these activation and repression inputs is required to establish the precise neuroectodermal pattern of huckebein, which is subsequently required for the development of specific neuroblast cell lineages [8].
• The sequential expression of hkb in selected cells of the primordia presages the sequence of cell movements [9].

Anatomical context of hkb

• In the posterior part of the blastoderm, hkb represses the expression of sna in the endodermal primordium (which we suggest to be adjacent to the mesodermal primordium) [10].
• Interacting functions of snail, twist and huckebein during the early development of germ layers in Drosophila [10].
• huckebein is required for glial development and axon pathfinding in the neuroblast 1-1 and neuroblast 2-2 lineages in the Drosophila central nervous system [11].
• Loss of huckebein does not switch these NBs into different NB fates, nor does it change the number of cells in their lineages; rather, it is required for glial development in the NB 1-1 lineage, and for axon pathfinding of a subset of interneurons and motoneurons in both lineages [11].

Associations of hkb with chemical compounds

• The engrailed and huckebein genes are essential for development of serotonin neurons in the Drosophila CNS [12].

Regulatory relationships of hkb

• Finally, we identify a novel pathway mediated by the gap gene huckebein through which three maternal systems cooperate to repress otd expression at the anterior terminus of the embryo [13].

Other interactions of hkb

• Instead, levels of Ras activity which suffice to drive tll and hkb transcription at the posterior pole fail to drive their expression in more central portions of the body, apparently due to repression by other gap gene products [14].
• Huckebein repressor activity in Drosophila terminal patterning is mediated by Groucho [15].
• The differentiation of the serotonergic neurons in the Drosophila ventral nerve cord depends on the combined function of the zinc finger proteins Eagle and Huckebein [6].
• Using an in vivo repression assay, we identify a functional repressor domain in Huckebein that contains an FRPW tetrapeptide, similar to the WRPW Groucho-recruitment domain found in Hairy-related repressor proteins [15].
• We suggest that mesodermal fate is determined where sna and twi but not hkb are expressed [10].

References