gurtelchen, gurt, 5953
tf - zinc finger - terminal gap gene - limits the extent of mesodermal development - required for proper endoderm formation
Please see the JBrowse view of Dmel\hkb for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.40
Gene model reviewed during 5.47
1.8 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
296 (aa)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\hkb using the Feature Mapper tool.
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as ventral nerve cord anlage
Comment: stripe of expression
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as salivary gland body specific anlage
hkb transcript disappears from the procephalic ectoderm by stage 11 and is restricted to neuroblasts derived from these regions. However, a lacZ reporter displays a longer perdurance in these regions. Expression in procephalic neuroblasts stage 9-11: tritocerebrum - d6, d8, v1; deuterocerebrum - d1-10, d12, d13, v1-v8; protocerebrum - cd2, cv7
hkb transcript is first detected in the salivary gland primordia in the posterior-most cells and then subsequently in dorsal-posterior cells that are the first to invaginate. There is also concomitant expression in a small group of cells in the dorsal-anterior region. Expression is higher in the dorsal aspect of the primordia but there is low level expression in the ventral region of the placode. hkb transcripts decreased and disappeared as invagination proceeded.
hkb transcript is expressed in two domains in the cellular balstoderm, forming an anterior and a posterior cap.
Expression of the terminal gap gene hkb is first detected in the anterior and posterior tips of the syncytial blastoderm. During gastrulation, hkb expression is shifted to a more ventral position so as to abut the invaginating ventral furrow. Later in gastrulation, the polar expression of hkb disappears. Instead, hkb transcript is present in the salivary gland placodes and in a metameric pattern in the developing CNS. hkb is expressed in the CNS through the rest of embryonic development. In hkb mutant embryos, the mesodermal and ectodermal primordia expand at the expense of the endoderm, indicating that hkb is required for endoderm development. When hkb is ectopically expressed in embryos, the expression of the central gap gene gt is reduced, and invagination of the ventral furrow is disrupted.
At the blastoderm stage, hkb protein is expressed in the anterior and posterior tips of the embryo, and at stage 7, it is expressed in the anterior and posterior midgut primordia. Starting at stage 8, until late stage 11, hkb protein is detected in the neurectoderm. hkb protein appears first in a neurectodermal cluster, then in the neuroblasts which laminate from that position, and finally in the early progenitors of these neuroblasts. The exception is neuroblast NB1-1, which begins expressing hkb protein partway through its development. hkb protein is detected in the central nervous system until the end of stage 16. hkb protein expression pattern closely matches the hkb transcript expression pattern, but the protein persists slightly longer than the RNA.
Comment: row 5
Comment: late stage 11
Comment: stripe of expression
Comment: reference states 5-5.5 hr AEL
Comment: reference states 5-5.5 hr AEL
Comment: reference states 5-5.5 hr AEL
Comment: reference states 5-5.5 hr AEL
Comment: late stage 11
Comment: late stage 11
GBrowse - Visual display of RNA-Seq signals
View Dmel\hkb in GBrowse 23-47.1
3-44.1
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
polyclonal
Source for merge of: hkb gurt
DNA-protein interactions: genome-wide binding profile assayed for hkb protein in 0-12 hr embryos; see mE1_TFBS_hkb collection report.
Internalisation of the salivary gland and salivary gland shape are altered in hkb mutant embryos.
hkb is required zygotically for the migration of the germ cells through the posterior midgut wall.
Mutants are isolated in an EMS mutagenesis screen to identify zygotic mutations affecting germ cell migration at discrete points during embryogenesis: mutants exhibit gut development defects.
The expression pattern of hkb protein during embryogenesis has been studied.
hkb is involved in regulation of serotonin cell development and has a role in neuronal identity subsequent to formation of neuroblast 7-3.
hkb is necessary for endoderm development and its activity defines the spatial limits within the blastoderm embryo in which the germ layers are established.
Mesodermal fate is determined where sna and twi but not hkb are expressed. Anteriorly, hkb together with sna determines endodermal fate, and hkb together with twi and sna are required for foregut development. hkb is a good candidate for factor X and factor Y, necessary for setting the anterior and posterior borders of the ventral furrow.
In mutant embryos, which do not form endodermal derivatives, germ band retraction is properly executed.
An artificial bcd responder gene composed of three bcd consensus binding sites driving Ecol\lacZ is activated by bcd and repressed by tor. This repression does not require tll or hkb.
Expression analysed in CNS study of neuroblasts and ganglion mother cells, using an enhancer trap to reveal the expression pattern.
In csw- embryos hb remains as a posterior cap and the seventh ftz stripe expands posteriorly, both due to lack of hkb repressing activity.
The activation and spatial limitation of tll and hkb expression in the posterior region of the embryo is critically dependent on tor activity. The spatial limitation of hkb and tll expression is not regulated by the "central gap genes" which are essential for the establishment of segmentation in the trunk of the embryo, and also does not involve mutual interactions between hkb and tll.
At the anterior end of the embryo tor effects on gt are mediated primarily through hkb.
Mutations in zygotic cardinal gene hkb do not interact with RpII140wimp.
hkb represses Kr expression in the central segmentation domain and activates Kr expression in the posterior Malpighian tubule domain.