High impact information on tll

• Kr activates stripe 5 and represses stripe 6, kni activates stripe 6 and represses stripe 7, and tll activates stripe 7 [1].
• That the tll gene may also play a role in the nervous system is suggested by its strong expression in the forming brain and transient expression in the peripheral nervous system [2].
• The Drosophila gene tailless is expressed at the embryonic termini and is a member of the steroid receptor superfamily [2].
• Ectopic expression of tll under the control of an inducible promoter results in differentiation of ectopic terminal-specific structures, the Filzkörper, and leads to the activation of at least one gene, hunchback, that is required to form these structures [3].
• Ectopic expression of the tll gene also represses segmentation by repressing the gap genes Krüppel and knirps and probably also pair rule genes [3].

Biological context of tll

• We show that the tll protein binds in vitro to specific sites within the 1.4 kb posterior enhancer region, providing the first direct evidence for activation of gene expression by tll [4].
• 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].
• Binding sites of bcd protein in a 0.5 kb region, revealed by DNaseI footprinting, could be crucial for the bcd-dependent activation of tll expression in the anterior stripe [6].
• The data presented here support a model in which activation of the tor RTK at the poles of the embryos leads to inactivation of the repressor and therefore, to transcriptional activation (by activators present throughout the embryo) of the tll gene at the poles of the embryo [7].
• Our analysis of the tor response element (tor-RE) in the tll promoter indicates that the key activity modulated by the tor RTK pathway is a repressor present throughout the embryo [7].

Anatomical context of tll

• Expression of tll is normally confined to the optic lobe primordium, whereas ato appears in a subset of Bolwig's organ cells that we call Bolwig's organ founders [8].
• 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 [9].
• The mouse homolog of the orphan nuclear receptor tailless is expressed in the developing forebrain [10].
• When Torso, which is uniformly distributed in the egg cell membrane, becomes activated locally at the termini, it triggers a phosphorylation cascade that culminates with localized expression of the transcription factors, tailless and huckebein [11].
• By marking cells of early gastrula stage embryos, we showed that in embryos mutant for a strong tll allele the fate map is shifted posteriorly and the hindgut anlage is deleted [12].

Associations of tll with chemical compounds

• Consistent with the rapid turnover of the tll protein, it contains a PEST sequence (rich in proline, glutamate and aspartate, serine, and threonine) that is also conserved [13].
• One of these residues, the alanine after the last cysteine in the first zinc finger, may be responsible for part of the difference between the tll protein DNA binding site and the closely related half-site of the retinoid/estrogen receptors [13].
• Consistent with the characterization of the tll protein as a putative transcription factor (a member of the steroid receptor superfamily) that represses segmentation genes and activates terminal-specific genes, we observe a correlation between the presence of the posterior cap of tll expression and differentiation of a telson [14].

Physical interactions of tll

• In vitro, all three HP1s bind to tailed and tailless nucleosomes and specifically interact with the histone-fold of histone H3 [15].

Regulatory relationships of tll

• Consistently, pole cells compromised for pgc function exhibit elevated levels of activated MAP kinase and premature transcription of the target gene tailless (tll) [16].
• bicoid and the terminal system activate tailless expression in the early Drosophila embryo [14].
• Transgenic reporter gene lines containing mutations of the TLL binding sites demonstrate that tll directly inhibits the expression of ems in the early embryonic head and the protocerebral brain anlage [17].
• Here, we show that a constitutively active form of human raf1 protein can trigger tll and hkb transcription in Drosophila embryos and specify elements of the terminal body pattern [18].
• Third, we mutated tailless lamin using two point mutations known to inhibit head-to-tail association of full-length lamin [19].

Other interactions of tll

• 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 [20].
• The regulators of tll expression in the embryonic visual system remain elusive, as we were unable to find evidence for regulation by the 'early eye genes' so, eya and ey, or by EGFR signaling [8].
• Loss of tll function results in the absence of all protocerebral neuroblasts, otd functions in a domain that includes a large part of the protocerebrum and a smaller part of the adjacent deuterocerebrum [21].
• This functional synergism between regulatory elements may play a role in the translation of the torso (tor) morphogen gradient into the sharp boundary of tll gene activity [6].
• Control of tailless expression by bicoid, dorsal and synergistically interacting terminal system regulatory elements [6].

Analytical, diagnostic and therapeutic context of tll

• Here, we studied by transmission electron microscopy which types of interaction are important for formation of protofilaments by a tailless lamin fragment derived from Drosophila lamin Dm0 [19].

References