A preliminary genetic analysis of TE146, a very large transposing element of Drosophila melanogaster

Gubb, David; Roote, John; Harrington, Glynnis; McGill, S; Durrant, Barabara; Shelton, M.; Ashburner, Michael

doi:10.1007/bf00328463

Cited by 15 publications

(14 citation statements)

References 31 publications

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“…Mutations and abbreviations not explained here are described in Lindsley and Zimm (36) and in FlyBase (37). The chromosomes used are as follows: two ethyl methylsulfonate-induced mutants of l (2) pr cn (38) and four deficiencies, Df(2L)TE146(Z)GW7 al dp b l(2)pwn cn [abbreviated GW7 (39)], Df(2L)b84h1 [abbreviated b84h1 (40)], Df(2L)b80e3, pr bw (abbreviated b80e3), and Df(2L)A400, b cn bw; T(2;3;4)CA4 [abbreviated A400 (41)]. …”

Section: Methodsmentioning

confidence: 99%

Microsatellite instability in Drosophila spellchecker1 (MutS homolog) mutants

Flores

Engels

1999

Proc. Natl. Acad. Sci. U.S.A.

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We have cloned a mutS homolog from Drosophila melanogaster called spellchecker1 (spel1) and have constructed spel1 mutant f lies. MutS proteins promote the correction of DNA mismatches and serve important roles in DNA replication, recombination, and repair. The spel1 gene belongs to a subfamily of mutS first characterized by the MSH2 gene of yeast and which also includes hMSH2, one of the two major hereditary nonpolyposis colon cancer loci of humans. Like msh2 mutants in other species, we find that f lies lacking the spel1 gene suffer a highly increased rate of instability in long runs of dinucleotide repeats when analyzed after 10-12 f ly generations. Using a new assay, we have also discovered that mutations in spel1 decrease the stability of a dinucleotide repeat when it is copied into the site of a double-strand break during gene conversion. Contrary to the case in mammalian cells, spel1 deficiency does not affect tolerance of f lies to a methylating agent nor does it affect resistance to ␥-irradiation.

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Section: Methodsmentioning

confidence: 99%

Microsatellite instability in Drosophila spellchecker1 (MutS homolog) mutants

Flores

Engels

1999

Proc. Natl. Acad. Sci. U.S.A.

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“…The following mutations and fly stocks were used in this study: as control or wild-type stocks we employed white 1118 (w 1118 ), w*; Kr If-1 /CyO P{Dfd-EYFP}2, Oregon-R or balanced sibling embryos. We used Df(2R)BSC281 as a deficiency for Ndg (Df Ndg); Df(2L)Exel7022, which deletes the two adjacent Drosophila type IV Collagen genes viking (vkg) and Col4a1 (previously referred to as Cg25C); Df(3L)Exel8101 as deficiency for Laminin A; Df(2L)TE35B-2 as deficiency for Laminin wing blister (Gubb et al, 1985); Df(3L)Exel6114 as Laminin B2 deficiency (Df LanB2); and Df(1)Exel6230, which removes the trol locus but also the adjacent segmentation gene giant. Mi{ET1}MB04184, P{hsILMiT} and P{Δ2-3}99B were used to generate the Ndg deletion alleles Ndg Δ0.4 and Ndg Δ1.4 (Fig.…”

Section: Fly Stocks and Geneticsmentioning

confidence: 99%

Characterization ofDrosophila Nidogen/entactinreveals roles in basement membrane stability, barrier function and nervous system patterning

et al. 2018

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Basement membranes (BMs) are specialized layers of extracellular matrix (ECM) mainly composed of Laminin, type IV Collagen, Perlecan and Nidogen/entactin (NDG). Recent in vivo studies challenged the initially proposed role of NDG as a major ECM linker molecule by revealing dispensability for viability and BM formation. Here, we report the characterization of the single Ndg gene in Drosophila. Embryonic Ndg expression was primarily observed in mesodermal tissues and the chordotonal organs, whereas NDG protein localized to all BMs. Although loss of Laminin strongly affected BM localization of NDG, Ndg-null mutants exhibited no overt changes in the distribution of BM components. Although Drosophila Ndg mutants were viable, loss of NDG led to ultrastructural BM defects that compromised barrier function and stability in vivo. Moreover, loss of NDG impaired larval crawling behavior and reduced responses to vibrational stimuli. Further morphological analysis revealed accompanying defects in the larval peripheral nervous system, especially in the chordotonal organs and the neuromuscular junction (NMJ). Taken together, our analysis suggests that NDG is not essential for BM assembly but mediates BM stability and ECMdependent neural plasticity during Drosophila development.

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“…The following mutations and fly stocks were used in this study: as control or wild-type stocks we employed white 1118 ( w 1118 ), w*; Kr lf-1 /CyO P{Dfd-EYFP}2, Oregon-R or balanced sibling embryos. We used Df(2R)BSC281 as a deficiency for Ndg (Df Ndg), Df(2L)Exel7022 which deletes the two adjacent Drosophila type IV Collagen genes viking (vkg) and Col4a1 (previously referred to as Cg25C), Df(3L)Exel8101 as deficiency for Laminin A, Df(2L)TE35B-2 as deficiency for Laminin wing blister (Gubb et al, 1985), Df(3L)Exel6114 as Laminin B2 deficiency (Df LanB2) and Df(1)Exel6230 that removes the trol locus but also the adjacent segmentation gene giant. Mi{ET1}MB04184, P{hsILMiT} and P(A2-3}99B were used to generate the Ndg deletion alleles Ndg A04 .…”

Section: Methodsmentioning

confidence: 99%

Characterization ofDrosophila Nidogen/entactinreveals roles in basement membrane stability, barrier function and nervous system plasticity

Wolfstetter

Dahlitz

Pfeifer

et al. 2018

Preprint

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Basement membranes (BMs) are specialized layers of extracellular matrix (ECM) mainly composed of Laminin, type IV Collagen, Perlecan and Nidogen/entactin (NDG). While the essential and evolutionary conserved functions of Laminin, Collagen and Perlecan are well documented in Drosophila and other species, the proposed role of NDG as the major ECM linker molecule has been challenged by several in vivo studies revealing that NDG is dispensable for viability and BM formation. Here, we report the characterization of the single Ndg gene in Drosophila. Embryonic Ndg expression differed from that of other BM components and was primarily observed in mesodermal tissues and the chordotonal organs, whereas NDG protein localized to all BMs. While loss of Laminin strongly affected BM-localization of NDG, Ndg null mutants exhibited no overt changes in the distribution of BM core components. However, loss of NDG led to ultrastructural BM defects compromising barrier function and stability in vivo. Although Ndg mutants were viable, loss of NDG led to decreased fecundity in flies as well as impaired crawling behavior and reduced response to vibrational stimuli in larvae. Further morphological analysis revealed accompanying defects in the larval peripheral nervous system especially in the chordotonal organs and the neuromuscular junction (NMJ), where Ndg genetically interacted with the Leukocyte-antigen-related-like (Lar) receptor gene to regulate NMJ extension and synaptic differentiation. Taken together, our analysis suggests that NDG is not essential for BM assembly but mediates BM stability and ECM-dependent neural plasticity during Drosophila development.Summary StatementIn this study we characterize Drosophila Nidogen/Entactin (Ndg) mutants revealing that loss of Ndg impairs basement membrane (BM) stability and permeability as well as proper function of the nervous system.

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A preliminary genetic analysis of TE146, a very large transposing element of Drosophila melanogaster

Cited by 15 publications

References 31 publications

Microsatellite instability in Drosophila spellchecker1 (MutS homolog) mutants

Microsatellite instability in Drosophila spellchecker1 (MutS homolog) mutants

Characterization ofDrosophila Nidogen/entactinreveals roles in basement membrane stability, barrier function and nervous system patterning

Characterization ofDrosophila Nidogen/entactinreveals roles in basement membrane stability, barrier function and nervous system plasticity

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