ri, radius incompletus
transcription factor - steroid receptor - zinc finger - a gap gene that later organizes the development of the second wing vein - Groucho corepressor functions as a cofactor for the Knirps short-range transcriptional repressor
Gene model reviewed during 5.46
Gene model reviewed during 5.55
None of the polypeptides share 100% sequence identity.
429 (aa); 45.6 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\kni using the Feature Mapper tool.
Comment: reported as head epidermis primordium
Comment: reported as head epidermis primordium
GBrowse - Visual display of RNA-Seq signalsView Dmel\kni in GBrowse 2
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.
Source for merge of: kni ri
dsRNA has been made from templates generated with primers directed against this gene. RNAi of kni causes dorsal overextension of primary dendrites in ddaD and ddaE neurons. For such neurons, the most distal branchpoint is located 25 microns or further from the distal tip of the primary dendrite. However, branching of these dendrites is almost completely blocked. RNAi also causes defects in muscle, defects in the epidermis and defects in dendrite morphogenesis.
knrl and kni possess multiple and redundant functions during tracheal development. knrl/ kni activity is necessary to mediate dpp signalling (which is required for tracheal cell migration and formation of dorsal and ventral branches). knrl/ kni activity in dorsal tracheal cells is essential for secondary and terminal branch formation, via repression of salm. The border between dorsal trunk and branch identity is established by the direct interaction of kni with a salm cis-regulatory element.
Zygotic activation of h stripe 6 expression is preceded by activation in response to maternal cad activity, activation does not depend exclusively on the zygotic activity of kni as thought previously. cad and kni activities cooperate in a non-synergistic manner to activate h stripe 6 transcription. Absence of kni does not cause lack of h stripe 6 activation but delays the appearance of the stripe. Activation of the stripe depends on a minimal number of activator binding sites that are scattered throughout the stripe 6 element.
In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.
Mutations in kni fail to complement ri, when rearranged with respect to each other, while complementing without rearrangement, suggesting ri-kni transvection. A kni cDNA transgene can rescue the ri phenotype. Genomic Southern data reveals that transheterozygosity of overlapping deficiencies resulting in an ri phenotype creates a small synthetic deletion in the kni upstream region.
Mutants are isolated in an EMS mutagenesis screen to identify zygotic mutations affecting germ cell migration at discrete points during embryogenesis: mutants exhibit gap pattern defects.
The eve stripe 2 enhancer and yeast Scer\FLP1-Scer\FRT system have been used to create a domain of ectopic kni expression in the blastoderm embryo. Specific disruptions of pair-rule patterning are correlated with the level and timing of ectopic expression. This suggests that the ectopic kni domain acts as a source for morphogenetic activity that specifies regions in the embryo where pair-rule genes can be activated or repressed.
The kni gene product mediates both transcriptional quenching and direct repression. The range of kni repression at upstream activators is ~50-100bp, leaving neighboring enhancers free to interact with the transcription complex. kni can also act in promoter-proximal positions, as a dominant repressor, where it can block multiple enhancers.
Gene product is known to regulate Kr CD (cis acting control element) expression.
Transcription factors hb and kni can associate with Kr in vitro and they interact functionally with Kr-dependent target gene expression mediated by a single Kr-binding site close to an heterologous promoter in Schneider cells.
The biochemically equivalent gene products of kni and knrl are both functional in the head anlage and lack of one gene can be overcome by the activity of the other. kni is also required for abdominal segmentation and knrl is nonfunctional in its posterior expression domain. Therefore the kni/knrl pair of genes provides a region-specific buffering system, rather than global functional redundancy.
Expression of prd depends on activation by gap gene hb, Kr, kni and gt products. Primary pair rule gene products act primarily in subsequent modulation rather than activation of prd stripes. Factors activating prd expression in the pair rule mode interact with those activating it along the dorso-ventral axis.
Evolutionary history for nuclear receptor genes, in which gene duplication events and swapping between domains of different origins took place, is studied.
4.4kb upstream sequence of kni directs Ecol\lacZ reporter gene constructs in a region corresponding to the endogenous kni transcripts. Deletion constructs were made to determine how kni is spatially regulated.
Males of an isogenic line with a mutation at the ri locus were treated with a standard light heat shock and by a heavy heat shock. Mass transposition of the copia-like element 412 occurred at five transposition "hot-spots" (43B, 49CD, 56A, 56E and 66A) when the F1 generation of males were crossed with untreated females of the same isogenic line. The probabilities of transposition were two orders of magnitude higher than in the control sample. Stepwise temperature treatment shows the induction depends on the intensity of the temperature than any other stress action.
kni is required to establish abdominal segmentation. knrl differs from kni with respect to transcription unit size, kni contains 1kb and knrl contains 19kb intron sequences. The consequence of the intron difference is that knrl cannot substitute for kni segmentation function. The length of the mitotic cycle provides physiological barrier to transcript size and could be a significant factor in controlling developmental gene activity during short phenocritical periods.
kni was included in a study to determine how gap genes influence gt expression.
kni is a dual regulator of gt in the embryo: represses in the head regions and maintains high levels of gt in the tail.
Zygotically active locus involved in the terminal developmental program in the embryo.
Mutations in ri affect individual longitudinal veins: vein specific effects.
kni mutants exhibit deletion of the abdomen.
ri, tg, tt, ab, cv, cv-2, cv-c and cv-d belong to the radius incompletus phenotypic group within the 'lack-of-vein' mutant class. Loss-of-function alleles at these loci remove stretches of veins in two or more longitudinal veins. Double mutants of this group have additive phenotypes suggesting the genes are vein-specific, and have small lanceolate wings. Genes are involved in whole vein region-specification rather than vein differentiation.
An investigation of the role of gap genes in expression from Ubx and Antp promoters in the blastoderm embryo reveals that a unique combination of gap genes and pair rule genes is required for their initial activation.
Mutations in kni alter gt expression in the posterior of the embryo.
Genetic analysis demonstrates that the effect of the gap gene product kni on homeotic gene expression in the visceral mesoderm is indirect and mediated by the genes that establish parasegment borders, eve and ftz.
kni activity exerts a negative effect on Antp expression. This negative regulation is indirect and mediated by an alteration of Kr expression, this can be seen when comparing Antp expression in kni- embryos and Kr-/kni- embryos. kni is involved in restricting Abd-B products within the A8--A9 domain.
Mutant embryos exhibit normal Dfd expression.
Mutant individuals display interruptions of wing vein L2.
Zygotic gap gene whose mutants are homozygous lethal; their denticle belts in segments one through seven are fused into a single field (Nusslein-Volhard and Wieschaus, 1980), but the head, thorax, eighth abdominal segment and tail region appear normal. Embryos homozygous for a strong kni mutant show a wide band of ftz staining instead of the normal number of ftz stripes (Carroll and Scott, 1986).