Rewiring of gene interactions during development of serially homologous appendages in male and female Drosophila
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PROVIDER: PRJNA1173189 | ENA |
REPOSITORIES: ENA
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Project description:Arthropod genitalia and walking legs are serially homologous appendages derived from a ventral appendage ‘ground state’ shaped by different Hox inputs. However, there has been little comparison between the downstream gene regulatory networks and how they build and pattern serially homologous appendages differently. In the pre-tarsal region of the developing leg and antennae of Drosophila, a combination of the transcription factors C15, Lim1 homeobox 1 (Lim1), and Al (Aristaless) are required for the development of the terminal structures, the tarsal claws and aristae, respectively, but the role and interactions among these factors as well as other genes known to regulate leg development was not known in the developing genitalia. Here, we explored the expression and function of C15, Lim1, and Al in male and female terminalia (genitalia and analia) development. We found that C15 represses male clasper bristle development but is required for promoting female epiproct bristles. Unlike in the antennae and leg discs, C15, Lim1, and Al are never all co-expressed in any male or female terminal structures, evidencing the interactions among these factors have changed among serially homologous appendages. However, we did infer interactions between C15 and other factors, including bab2 and Dll reflecting similarities between leg and genital development consistent with their homology. Finally, we identified a male-specific clasper enhancer of C15, probably regulated by the Hox gene Abdominal-B, which is not active in the female terminalia or the legs or antennae. This enhancer modularity of C15 may underpin tissue-specific regulatory logic, presumably programmed by different Hox inputs such as Abd-B in the genitalia, and that could have contributed to the diversification of these serially homologous structures from the ‘ground state’ ventral appendage as well as the rapid evolution of terminal morphology among species.
2024-10-21 | GSE279524 | GEO
Project description:Homologous recombination is essential for high-fidelity DNA repair during mitotic proliferation and meiosis. Yet, context-specific modifications must tailor the recombination machinery to avoid, or enforce, formation of reciprocal exchanges – crossovers – between recombining chromosomes. To obtain molecular insight into how crossover control is achieved, we affinity-purified the 7 DNA-processing enzymes with known roles in channelling HR intermediates into crossovers, or non-crossovers, from vegetative cells, or cells undergoing meiosis. Using mass spectrometry, we provide the first global characterization of their composition. The resulting mitosis- and meiosis-specific interaction maps reveal intricate changes in enzyme architecture and a concerted rewiring of the interaction networks to support flexible control to the recombination outcome. Moreover, functional analyses of 31 novel interactions uncovered 8 meiosis-specific network components that remodel HR to support crossing-over. Chd1, which transiently associates with Exo1 during meiosis, enables the formation of MutLγ-Exo1-dependent crossovers through its conserved ability to bind and displace nucleosomes.
2019-07-31 | PXD012486 | Pride
Project description:We mapped open chromatin by FAIRE-seq and measured gene expression by RNA-seq in 3 types of Drosophila samples: staged whole embryos, imaginal discs, pharate appendages. We first demonstrate that regions of open chromatin precisely define regions of enhancer activity in developing embryos. In contrast to the dynamic changes in open chromatin observed between different stages of embryogenesis, we found that the open chromatin profiles in wing, leg, and haltere imaginal discs are nearly identical. This was also true again later in development, where the adult appendages also share nearly identical open chromatin profiles. Therefore, at a given developmental time point, different appendages are specified using a shared set of DNA regulatory elements. However, from one time point to the next, the set of accessible regulatory elements changes. Open chromatin profiles in appendage imaginal discs are almost entirely different than those of the adult appendages. We propose that master regulator transcription factors create morphologically distinct structures by differentially influencing the function of the same set of DNA regulatory modules. Open chromatin profiling during Drosophila development: 3 stages of embryogenesis (2-replicates each); wing, leg, and haltere 3rd instar imaginal discs (3-replicates each); 3rd larval central nervous system (2-replicates); eye-antennal imaginal discs (2-replicates); wing, leg, and haltere pharate appendages (2-replicates each); Genomic DNA Inputs. Sequencing performed on Illumina GAII and HiSeq.
2013-11-07 | E-GEOD-38727 | biostudies-arrayexpress
Project description:We mapped open chromatin by FAIRE-seq and measured gene expression by RNA-seq in 3 types of Drosophila samples: staged whole embryos, imaginal discs, pharate appendages. We first demonstrate that regions of open chromatin precisely define regions of enhancer activity in developing embryos. In contrast to the dynamic changes in open chromatin observed between different stages of embryogenesis, we found that the open chromatin profiles in wing, leg, and haltere imaginal discs are nearly identical. This was also true again later in development, where the adult appendages also share nearly identical open chromatin profiles. Therefore, at a given developmental time point, different appendages are specified using a shared set of DNA regulatory elements. However, from one time point to the next, the set of accessible regulatory elements changes. Open chromatin profiles in appendage imaginal discs are almost entirely different than those of the adult appendages. We propose that master regulator transcription factors create morphologically distinct structures by differentially influencing the function of the same set of DNA regulatory modules.
2013-11-07 | GSE38727 | GEO
Project description:This DNA methylation dataset describes epigenomic changes in in vitro serially passaged primary and immortalized astrocytes, in the context of studies examining cellular aging patterns that are conserved in vivo and in vitro. Primary and fetal hTERT-immortalized astrocytes were grown under normoxic conditions and serially passaged. Longitudinal DNA samples were collected throughout passaging and DNA methylation was measured using the Infinium HumanMethylation850 BeadChip.
2023-07-21 | GSE226079 | GEO
Project description:Mitosis segregates into each daughter cell two centrioles, the older of which is uniquely capable of generating a cilium. How this older centriole, called the mother centriole, initiates ciliogenesis remains poorly understood. We have identified an evolutionarily conserved complex comprised of CEP90, OFD1, MNR and FOPNL. Human mutations in CEP90, MNR and OFD1 cause ciliopathies. Super-resolution microscopy revealed that this complex forms a ring at the distal centriole. Centrioles of cells lacking MNR or CEP90 failed to assemble distal appendages and cannot generate cilia. In addition to the centrioles, complex members localized to centriolar satellites, proteinaceous granules surrounding the centrioles. Disruption of satellites did not affect distal appendage assembly, indicating that the centriolar pool is required for ciliogenesis. Consistent with an essential role in ciliogenesis, mice lacking MNR or CEP90 did not assemble cilia, did not survive beyond embryonic day 9.5, and did not transduce Hedgehog signals. In addition to ciliogenesis, MNR, but not CEP90, restrained centriolar length. MNR recruited both OFD1, required for centriolar length control, and CEP90, which recruits CEP83 to root distal appendages. Thus, an evolutionarily conserved ciliopathy-associated complex functions at the distal centriole to control centriole length and assemble distal appendages.
2021-06-15 | PXD022372 | Pride
Project description:Sex-specific gene expression in sensory organs may play an important role in mating and foraging behavior. We used long-oligonucleotide microarrays to compare gene expression profiles of males and females in three adult appendages that carry large numbers of chemosensory organs – antenna, proboscis, and front leg. Keywords: tissue-specific expression profiles
2007-06-22 | GSE5189 | GEO
Project description:Nosocomial pathogens serially passaged in silver nitrate (Raw sequence reads)
| PRJNA692851 | ENA
Project description:Homologous pairing and synapsis are essential in meiotic prophase I during spermatogenesis. However, the underlying mechanisms of how alternative splicing (AS) functions in homologous pairing and synapsis remain largely unclear. We reveal that SRSF1 is essential for gene expression and AS in homologous pairing and synapsis. Conditional knockout (cKO) of Srsf1 in mouse germ cells impaired homologous pairing and synapsis, leading to non-obstructive azoospermia (NOA). SRSF1 was required for initial homology recognition, telomere-led chromosome movement, and synaptonemal complex (SC) assembly. Moreover, SRSF1 interacted with TRA2B and U2AF2, directly binding and regulating the expression of Dmc1, Sycp1, Sun1, and Majin via AS to implement homologous pairing and synapsis during the meiotic prophase I program. Altogether, our data reveal the critical role of an SRSF1-mediated post-transcriptional regulatory mechanism in homologous pairing and synapsis during meiotic prophase I, providing a framework for elucidating the molecular mechanisms underlying the post-transcriptional network of male meiosis.
2024-01-09 | GSE227403 | GEO
Project description:Homologous pairing and synapsis are essential in meiotic prophase I during spermatogenesis. However, the underlying mechanisms of how alternative splicing (AS) functions in homologous pairing and synapsis remain largely unclear. We reveal that SRSF1 is essential for gene expression and AS in homologous pairing and synapsis. Conditional knockout (cKO) of Srsf1 in mouse germ cells impaired homologous pairing and synapsis, leading to non-obstructive azoospermia (NOA). SRSF1 was required for initial homology recognition, telomere-led chromosome movement, and synaptonemal complex (SC) assembly. Moreover, SRSF1 interacted with TRA2B and U2AF2, directly binding and regulating the expression of Dmc1, Sycp1, Sun1, and Majin via AS to implement homologous pairing and synapsis during the meiotic prophase I program. Altogether, our data reveal the critical role of an SRSF1-mediated post-transcriptional regulatory mechanism in homologous pairing and synapsis during meiotic prophase I, providing a framework for elucidating the molecular mechanisms underlying the post-transcriptional network of male meiosis.
2024-01-08 | GSE227303 | GEO