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The Drosophila Pax6 paralogs have different functions in head development but can partially substitute for each other
Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). (Åsa Rasmuson-Lestander)
Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). (Umeå University Umeå Centre for Molecular Pathogenesis 901 87 Umeå Sweden)
Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). (Rasmuson)
2009 (Engelska)Ingår i: Molecular Genetics and Genomics, ISSN 1617-4615, E-ISSN 1617-4623, Vol. 282, nr 3, s. 217-231Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

There are two Pax6 genes in Drosophila melanogaster; eyeless (ey) and twin-of-eyeless (toy), due to a duplication, which most likely occurred in the insect lineage. They encode transcription factors important for head development. Misexpression of either toy or ey can induce formation of ectopic compound eyes. Toy regulates the ey gene by binding to an eye-specific enhancer in its second intron. However, Toy can induce ectopic eyes also in an ey( - ) background, which indicates a redundancy between the two Pax6 copies in eye formation. To elucidate to what extent these two genes are interchangeable, we first generated toy-Gal4 constructs capable of driving the Pax6 genes in a toy-specific manner. Genetic dissection of the promoter proximal region of toy identified a 1,300-bp region around the canonical transcription start that is sufficient to drive toy expression in embryonic brain and eye primorida and in larval eye-antennal discs. We find that exogenous expression of toy can partially rescue the lethality and eye phenotype caused by lethal mutations in ey and vice versa. We therefore conclude that Toy and Ey, to some extent, can substitute for each other. Nevertheless, the phenotypes of the rescued flies indicate that the two Pax6 genes are specialized to regulate defined structures of the fly head.

Ort, förlag, år, upplaga, sidor
2009. Vol. 282, nr 3, s. 217-231
Nyckelord [en]
Pax6 - Twin-of-eyeless - Eyeless - Mutant rescue - Drosophila
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:umu:diva-33092DOI: 10.1007/s00438-009-0458-2PubMedID: 19484263Scopus ID: 2-s2.0-69249209831OAI: oai:DiVA.org:umu-33092DiVA, id: diva2:310049
Tillgänglig från: 2010-04-12 Skapad: 2010-04-12 Senast uppdaterad: 2023-03-24Bibliografiskt granskad
Ingår i avhandling
1. Regulation and function of Pax-6 during head and eye development in Drosophila melanogaster
Öppna denna publikation i ny flik eller fönster >>Regulation and function of Pax-6 during head and eye development in Drosophila melanogaster
2012 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

In Drosophila melanogaster, eyeless and twin of eyeless have important function during eye development. Mutants of both genes give a variety of eye and head phenotypes with the strongest being almost headless meaning that they lack all structures derived from the eye-antennal disc. toy the first eye specification gene expressed in the regulatory network that leads to eye formation and the gene actvates eyeless. What regulates toy is still not clear and has been the focus of this thesis. In Paper I, we analysed part of the upstream region of the toy gene to be able to drive reporter genes with the expected expression pattern in embyo and larval tissues. We found that a 1300-bp region surrounding the toy transcription start is important for correct Toy expression during embryonic and larval development. We also tested for possible redundancy between the toy and ey genes by rescue experiments on some lethal allels in both genes and found that Pax-6 proteins can substitute for each other concerning both head structures and survival. However, rescue is only partial, indicating that the proteins are not fully compatible or that the levels of expression are not sufficiently reproduced by the artificial Gal4-UAS system. Furthermore, we show that inhibition of apoptosis increased survival in strong toy mutants, but did not improve eye phenotypes. In Paper II, we searched for possibly upstream regulators of toy and found that the head gap gene empty spiracles changed the expression pattern of Toy significantly in the embryonic eye-antennal primordium. By clonal analysis and ectopic expressions, we made the conclusion that Ems acts as a repressor of toy during late embryonic development and also at later developmental stages. In Paper III, we investigate presumptive toy enhancer regions within the intron sequences of the gene. Generation and examination of transgenic lines showed that there might be an enhancer region driving toy expression in the embryonic ventral nerve cord within intron 2.

Ort, förlag, år, upplaga, sidor
Umeå: Umeå universitet, 2012. s. 40
Nationell ämneskategori
Naturvetenskap
Forskningsämne
molekylärbiologi
Identifikatorer
urn:nbn:se:umu:diva-50742 (URN)978-91-7459-348-8 (ISBN)
Disputation
2012-01-20, KBC-huset, Stora hörsalen KB3B1, Umeå universitet, Umeå, 09:00 (Engelska)
Opponent
Handledare
Tillgänglig från: 2011-12-21 Skapad: 2011-12-20 Senast uppdaterad: 2018-06-08Bibliografiskt granskad

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Jacobsson, LinnKronhamn, JesperRasmuson-Lestander, Åsa

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Jacobsson, LinnKronhamn, JesperRasmuson-Lestander, Åsa
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Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet)Institutionen för molekylärbiologi (Medicinska fakulteten)
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Molecular Genetics and Genomics
Medicin och hälsovetenskap

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