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János Szabad

Researcher at University of Szeged

Publications -  59
Citations -  2390

János Szabad is an academic researcher from University of Szeged. The author has contributed to research in topics: Drosophila melanogaster & Gene. The author has an hindex of 23, co-authored 59 publications receiving 2304 citations. Previous affiliations of János Szabad include MTA Biological Research Centre & University of Zurich.

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A gain-of-function mutation in Drosophila MAP kinase activates multiple receptor tyrosine kinase signaling pathways

TL;DR: A gain-of-function mutation in rolled is identified (rlSevenmaker [rlSem], which encodes a homolog of mitogen-activated protein (MAP) kinase, which activation of MAP kinase by the rlSem mutation is both necessary and sufficient to activate multiple signaling pathways controlled by receptor tyrosine kinases.
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Function of torso in determining the terminal anlagen of the Drosophila embryo.

TL;DR: The tor gain-of-function effect is neutralized, and segmentation is restored in double mutants with the zygotic gene tailless4,5 (tll), which has a phenotype similar to that of tor–, suggesting that tor acts through tll, and that in the gain- of-function alleles of tor, the tll gene product is ectopically expressed at middle positions of the embryo, where it inhibits the expression of segmentation genes like ftz.
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The development and function of the female germ line in Drosophila melanogaster: A cell lineage study

TL;DR: X-ray-induced mitotic recombination was used to follow the development and function of the female germ line in Drosophila melanogaster and indicated that the stem cell divisions characteristic of the adult period have begun shortly after pupation.
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Autophagy in Drosophila ovaries is induced by starvation and is required for oogenesis.

TL;DR: It is shown that starvation induces autophagy in germline cells (GCs) and in follicle cells (FCs) in Drosophila ovaries and this process is mediated by the ATG machinery and involves the upregulation of Atg genes, and it is demonstrated that insulin/TOR signaling controls autophagic in FCs and GCs.
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TPPP/p25 promotes tubulin assemblies and blocks mitotic spindle formation

TL;DR: Injection of bovine TPPP/p25 into cleavage Drosophila embryos expressing tubulin–GFP fusion protein reveals that TPPP-p25 inhibits mitotic spindle assembly and nuclear envelope breakdown without affecting other cellular events like centrosome replication and separation, microtubule nucleation by the centrosomes, and nuclear growth.