@article{MTMT:34772438, title = {Mitochondrial Differentiation during Spermatogenesis: Lessons from Drosophila melanogaster}, url = {https://m2.mtmt.hu/api/publication/34772438}, author = {Vedelek, Viktor and Jankovics, Ferenc and Zádori, János and Sinka, Rita}, doi = {10.3390/ijms25073980}, journal-iso = {INT J MOL SCI}, journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}, volume = {25}, unique-id = {34772438}, issn = {1661-6596}, abstract = {Numerous diseases can arise as a consequence of mitochondrial malfunction. Hence, there is a significant focus on studying the role of mitochondria in cancer, ageing, neurodegenerative diseases, and the field of developmental biology. Mitochondria could exist as discrete organelles in the cell; however, they have the ability to fuse, resulting in the formation of interconnected reticular structures. The dynamic changes between these forms correlate with mitochondrial function and mitochondrial health, and consequently, there is a significant scientific interest in uncovering the specific molecular constituents that govern these transitions. Moreover, the specialized mitochondria display a wide array of variable morphologies in their cristae formations. These inner mitochondrial structures are closely associated with the specific functions performed by the mitochondria. In multiple cases, the presence of mitochondrial dysfunction has been linked to male sterility, as it has been observed to cause a range of abnormal spermatogenesis and sperm phenotypes in different species. This review aims to elucidate the dynamic alterations and functions of mitochondria in germ cell development during the spermatogenesis of Drosophila melanogaster.}, year = {2024}, eissn = {1422-0067}, orcid-numbers = {Vedelek, Viktor/0000-0002-0420-8226; Sinka, Rita/0000-0003-4040-4184} } @article{MTMT:34575637, title = {Direct interaction of Su(var)2-10 via the SIM-binding site of the Piwi protein is required for transposon silencing in Drosophila melanogaster}, url = {https://m2.mtmt.hu/api/publication/34575637}, author = {Bence, Melinda and Jankovics, Ferenc and Kristó, Ildikó and Gyetvai, Akos and Vértessy, Beáta (Grolmuszné) and Erdélyi, Miklós}, doi = {10.1111/febs.17073}, journal-iso = {FEBS J}, journal = {FEBS JOURNAL}, unique-id = {34575637}, issn = {1742-464X}, abstract = {Nuclear Piwi/Piwi-interacting RNA complexes mediate co-transcriptional silencing of transposable elements by inducing local heterochromatin formation. In Drosophila, sumoylation plays an essential role in the assembly of the silencing complex; however, the molecular mechanism by which the sumoylation machinery is recruited to the transposon loci is poorly understood. Here, we show that the Drosophila E3 SUMO-ligase Su(var)2-10 directly binds to the Piwi protein. This interaction is mediated by the SUMO-interacting motif-like (SIM-like) structure in the C-terminal domain of Su(var)2-10. We demonstrated that the SIM-like structure binds to a special region found in the MID domain of the Piwi protein, the structure of which is highly similar to the SIM-binding pocket of SUMO proteins. Abrogation of the Su(var)2-10-binding surface of the Piwi protein resulted in transposon derepression in the ovary of adult flies. Based on our results, we propose a model in which the Piwi protein initiates local sumoylation in the silencing complex by recruiting Su(var)2-10 to the transposon loci.}, keywords = {SUBSTRATE; Drosophila melanogaster; Defense; MOTIF; Sumoylation; Sumoylation; SUMO; piRNA pathway; Su(var)2-10; PIWI/piRNA; ENFORCES}, year = {2024}, eissn = {1742-4658} } @CONFERENCE{MTMT:34689202, title = {Studying Drosophila blood cell plasticity using primary blood cell cultures}, url = {https://m2.mtmt.hu/api/publication/34689202}, author = {Kúthy-Sutus, Enikő and Gábor, Erika and Kharrat, Bayan and Jankovics, Ferenc and Sinka, Rita and Honti, Viktor}, booktitle = {Straub-Napok 2022}, unique-id = {34689202}, year = {2022}, pages = {1}, orcid-numbers = {Kúthy-Sutus, Enikő/0000-0002-1398-4120; Sinka, Rita/0000-0003-4040-4184} } @article{MTMT:33025619, title = {Characterization and functional analysis of zinc trafficking in the human fungal pathogen Candida parapsilosis}, url = {https://m2.mtmt.hu/api/publication/33025619}, author = {Takács, Tamás and Németh, Tibor Mihály and Bohner, Flóra and Vágvölgyi, Csaba and Jankovics, Ferenc and Wilson, Duncan and Gácser, Attila}, doi = {10.1098/rsob.220077}, journal-iso = {OPEN BIOL}, journal = {OPEN BIOLOGY}, volume = {12}, unique-id = {33025619}, abstract = {The zinc restriction and zinc toxicity are part of host defence, called nutritional immunity. The crucial role of zinc homeostasis in microbial survival within a host is established, but little is known about these processes in the opportunistic human fungal pathogen Candida parapsilosis. Our in silico predictions suggested the presence of at least six potential zinc transporters (ZnTs) in C. parapsilosis-orthologues of ZRC1, ZRT3 and ZRT101-but an orthologue of PRA1 zincophore was not found. In addition, we detected a species-specific gene expansion of the novel ZnT ZRT2, as we identified three orthologue genes in the genome of C. parapsilosis. Based on predictions, we created homozygous mutant strains of the potential ZnTs and characterized them. Despite the apparent gene expansion of ZRT2 in C. parapsilosis, only CpZRT21 was essential for growth in a zinc-depleted acidic environment, in addition we found that CpZrc1 is essential for zinc detoxification and also protects the fungi against the elimination of murine macrophages. Significantly, we demonstrated that C. parapsilosis forms zincosomes in a Zrc1-independent manner and zinc detoxification is mediated by the vacuolar importer CpZrc1. Our study defines the functions of C. parapsilosis ZnTs, including a species-specific survival and zinc detoxification system.}, keywords = {GENE; RESISTANCE; TRANSPORTERS; Virulence; ZINC; PATHOGEN; STORAGE; Candida; vacuole; intracellular zinc; ZRC1}, year = {2022}, eissn = {2046-2441}, orcid-numbers = {Vágvölgyi, Csaba/0000-0003-0009-7773} } @article{MTMT:32990099, title = {Drosophila MESR4 Gene Ensures Germline Stem Cell Differentiation by Promoting the Transcription of bag of marbles}, url = {https://m2.mtmt.hu/api/publication/32990099}, author = {Szarka-Kovács, Alexandra Brigitta and Takács, Zsanett and Bence, Melinda and Erdélyi, Miklós and Jankovics, Ferenc}, doi = {10.3390/cells11132056}, journal-iso = {CELLS-BASEL}, journal = {CELLS}, volume = {11}, unique-id = {32990099}, abstract = {Ovarian germline stem cells (GSCs) of Drosophila melanogaster provide a valuable in vivo model to investigate how the adult stem cell identity is maintained and the differentiation of the daughter cells is regulated. GSCs are embedded into a specialized cellular microenvironment, the so-called stem cell niche. Besides the complex signaling interactions between the germ cells and the niche cells, the germ cell intrinsic mechanisms, such as chromatin regulation and transcriptional control, are also crucial in the decision about self-renewal and differentiation. The key differentiation regulator gene is the bag of marbles (bam), which is transcriptionally repressed in the GSCs and de-repressed in the differentiating daughter cell. Here, we show that the transcription factor MESR4 functions in the germline to promote GSC daughter differentiation. We find that the loss of MESR4 results in the accumulation of GSC daughter cells which fail to transit from the pre-cystoblast (pre-CB) to the differentiated cystoblast (CB) stage. The forced expression of bam can rescue this differentiation defect. By a series of epistasis experiments and a transcriptional analysis, we demonstrate that MESR4 positively regulates the transcription of bam. Our results suggest that lack of repression alone is not sufficient, but MESR4-mediated transcriptional activation is also required for bam expression.}, keywords = {EXPRESSION; MECHANISMS; PATHWAY; DROSOPHILA; DIVISION; MAINTENANCE; ovary; germ cell; Stem Cell Niche; finger; SELF-RENEWAL; PHD; Stem cell differentiation; germline stem cell; Plant homeodomain; bag of marbles}, year = {2022}, eissn = {2073-4409} } @article{MTMT:31148157, title = {The SUMO Ligase Su(var)2-10 Controls Hetero- and Euchromatic Gene Expression via Establishing H3K9 Trimethylation and Negative Feedback Regulation.}, url = {https://m2.mtmt.hu/api/publication/31148157}, author = {Ninova, Maria and Godneeva, Baira and Chen, Yung-Chia Ariel and Luo, Yicheng and Prakash, Sharan J and Jankovics, Ferenc and Erdélyi, Miklós and Aravin, Alexei A and Fejes Tóth, Katalin}, doi = {10.1016/j.molcel.2019.09.033}, journal-iso = {MOL CELL}, journal = {MOLECULAR CELL}, volume = {77}, unique-id = {31148157}, issn = {1097-2765}, abstract = {Сhromatin is critical for genome compaction and gene expression. On a coarse scale, the genome is divided into euchromatin, which harbors the majority of genes and is enriched in active chromatin marks, and heterochromatin, which is gene-poor but repeat-rich. The conserved molecular hallmark of heterochromatin is the H3K9me3 modification, which is associated with gene silencing. We found that in Drosophila, deposition of most of the H3K9me3 mark depends on SUMO and the SUMO ligase Su(var)2-10, which recruits the histone methyltransferase complex SetDB1/Wde. In addition to repressing repeats, H3K9me3 influences expression of both hetero- and euchromatic host genes. High H3K9me3 levels in heterochromatin are required to suppress spurious transcription and ensure proper gene expression. In euchromatin, a set of conserved genes is repressed by Su(var)2-10/SetDB1-induced H3K9 trimethylation, ensuring tissue-specific gene expression. Several components of heterochromatin are themselves repressed by this pathway, providing a negative feedback mechanism to ensure chromatin homeostasis.}, keywords = {Chromatin; gene regulation; epigenetics; TRANSCRIPTIONAL REPRESSION; HETEROCHROMATIN; GERMLINE; SUMO; transposons; H3K9me3; cell fate maintenance}, year = {2020}, eissn = {1097-4164}, pages = {571-585} } @article{MTMT:30585796, title = {Headcase is a Repressor of Lamellocyte Fate in Drosophila melanogaster}, url = {https://m2.mtmt.hu/api/publication/30585796}, author = {Varga, Gergely István and Csordás, Gábor and Cinege, Gyöngyi Ilona and Jankovics, Ferenc and Sinka, Rita and Kurucz, Judit Éva and Andó, István and Honti, Viktor}, doi = {10.3390/genes10030173}, journal-iso = {GENES-BASEL}, journal = {GENES}, volume = {10}, unique-id = {30585796}, issn = {2073-4425}, abstract = {Due to the evolutionary conservation of the regulation of hematopoiesis, Drosophila provides an excellent model organism to study blood cell differentiation and hematopoietic stem cell (HSC) maintenance. The larvae of Drosophila melanogaster respond to immune induction with the production of special effector blood cells, the lamellocytes, which encapsulate and subsequently kill the invader. Lamellocytes differentiate as a result of a concerted action of all three hematopoietic compartments of the larva: the lymph gland, the circulating hemocytes, and the sessile tissue. Within the lymph gland, the communication of the functional zones, the maintenance of HSC fate, and the differentiation of effector blood cells are regulated by a complex network of signaling pathways. Applying gene conversion, mutational analysis, and a candidate based genetic interaction screen, we investigated the role of Headcase (Hdc), the homolog of the tumor suppressor HECA in the hematopoiesis of Drosophila. We found that naive loss-of-function hdc mutant larvae produce lamellocytes, showing that Hdc has a repressive role in effector blood cell differentiation. We demonstrate that hdc genetically interacts with the Hedgehog and the Decapentaplegic pathways in the hematopoietic niche of the lymph gland. By adding further details to the model of blood cell fate regulation in the lymph gland of the larva, our findings contribute to the better understanding of HSC maintenance.}, keywords = {DIFFERENTIATION; DROSOPHILA; innate immunity; blood cell; niche; Hematopoiesis; Hemocyte}, year = {2019}, eissn = {2073-4425}, orcid-numbers = {Varga, Gergely István/0000-0001-9073-5788; Csordás, Gábor/0000-0001-6871-6839; Sinka, Rita/0000-0003-4040-4184; Andó, István/0000-0002-4648-9396} } @article{MTMT:30377083, title = {Drosophila small ovary gene is required for transposon silencing and heterochromatin organization, and ensures germline stem cell maintenance and differentiation}, url = {https://m2.mtmt.hu/api/publication/30377083}, author = {Jankovics, Ferenc and Bence, Melinda and Sinka, Rita and Faragó, Anikó and Bodai, László and Pettkó-Szandtner, Aladár and Ibrahim, Karam and Takács, Zsanett and Szarka-Kovács, Alexandra Brigitta and Erdélyi, Miklós}, doi = {10.1242/dev.170639}, journal-iso = {DEVELOPMENT}, journal = {DEVELOPMENT}, volume = {145}, unique-id = {30377083}, issn = {0950-1991}, abstract = {Self-renewal and differentiation of stem cells is one of the fundamental biological phenomena relying on proper chromatin organization. In our study, we describe a novel chromatin regulator encoded by the Drosophila small ovary (sov) gene. We demonstrate that soy is required in both the germline stem cells (GSCs) and the surrounding somatic niche cells to ensure GSC survival and differentiation. soy maintains niche integrity and function by repressing transposon mobility, not only in the germline, but also in the soma. Protein interactome analysis of Sov revealed an interaction between Sov and HP1a. In the germ cell nuclei, Soy colocalizes with HP1a, suggesting that Sov affects transposon repression as a component of the heterochromatin. In a position-effect variegation assay, we found a dominant genetic interaction between soy and HP1a, indicating their functional cooperation in promoting the spread of heterochromatin. An in vivo tethering assay and FRAP analysis revealed that Sov enhances heterochromatin formation by supporting the recruitment of HP1a to the chromatin. We propose a model in which soy maintains GSC niche integrity by regulating transposon silencing and heterochromatin formation.}, keywords = {EXPRESSION; DROSOPHILA; Chromatin; PHASE-SEPARATION; Stem Cell Niche; HETEROCHROMATIN; HISTONE H3; SELF-RENEWAL; piRNA; WIDE RNAI SCREEN; BAG-OF-MARBLES; PIRNA BIOGENESIS; MEIOTIC CHECKPOINT; PIWI}, year = {2018}, eissn = {1477-9129}, orcid-numbers = {Jankovics, Ferenc/0000-0001-9697-4472; Sinka, Rita/0000-0003-4040-4184; Bodai, László/0000-0001-8411-626X} } @article{MTMT:30362934, title = {Headcase, a novel regulator of hemocyte differentiation in Drosophila Melanogaster}, url = {https://m2.mtmt.hu/api/publication/30362934}, author = {Varga, Gergely István and Csordás, Gábor and Jankovics, Ferenc and Lukacsovich, Tamás and Cinege, Gyöngyi Ilona and Sinka, Rita and Kurucz, Judit Éva and Andó, István and Honti, Viktor}, journal-iso = {IMMUNOLÓGIAI SZEMLE}, journal = {IMMUNOLÓGIAI SZEMLE}, volume = {10}, unique-id = {30362934}, issn = {2061-0203}, year = {2018}, pages = {51-51}, orcid-numbers = {Varga, Gergely István/0000-0001-9073-5788; Csordás, Gábor/0000-0001-6871-6839; Sinka, Rita/0000-0003-4040-4184; Andó, István/0000-0002-4648-9396} } @article{MTMT:3232089, title = {The actin binding cytoskeletal protein Moesin is involved in nuclear mRNA export}, url = {https://m2.mtmt.hu/api/publication/3232089}, author = {Kristó, Ildikó and Bajusz, Csaba and Borsos, Barbara Nikolett and Pankotai, Tibor and Dopie, Joseph and Jankovics, Ferenc and Vartiainen, Maria K and Erdélyi, Miklós and Vilmos, Péter}, doi = {10.1016/j.bbamcr.2017.05.020}, journal-iso = {BBA-MOL CELL RES}, journal = {BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH}, volume = {1864}, unique-id = {3232089}, issn = {0167-4889}, year = {2017}, eissn = {1879-2596}, pages = {1589-1604}, orcid-numbers = {Pankotai, Tibor/0000-0001-9810-5465} }