The Department of Cell and Developmental Biology actively participates in teaching in the human medicine (histology) and medical informatics curriculum. The scientific and research activities of the various working groups focus on the following research areas:
Copy Number Determination of Sperm-Borne Small RNAs Implied in the Intergenerational Inheritance of Metabolic Syndromes
Mammalian spermatocytes harbour small RNAs that have been implicated in inheriting paternally acquired traits in rodents. How these paternally transmitted small RNAs could function mechanistically in the developing zygote remains to be understood. Since nothing is known about how many small RNAs are required for functional impact, the Schaefer and Wossidlo labs, in collaboration with others, determined the copy numbers of specific small RNAs contained in a single spermatocyte. The results underscore the need for better quantitative insights before using non-physiological copy numbers of small RNAs in the manipulation of a biological system.
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Eosinophil innate immune memory after bacterial skin infection promotes allergic lung inflammation
The Sombke group contributed to a collaborative effort that aimed at understanding how microbial exposures affect the later development of immune pathologies such as autoimmunity and allergies. Using a mouse model of Staphylococcus aureus infection, this study reports that skin bacterial infection enhanced sensitization to cutaneous allergen, which subsequently worsened allergic lung inflammation.
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tRNA expression and modification landscapes, and their dynamics during zebrafish embryo development
In a collaborative effort, the Vilardo group analysed nucleo-cytoplasmic and mitochondrial tRNAs during embryonic development of the model vertebrate zebrafish. Their findings suggest the existence of a general reprogramming of the expressed tRNA pool, possibly gearing the translational machinery for distinct stages of the delicate and crucial process of embryo development.
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RNA Pol II-dependent transcription efficiency fine-tunes A-to-I editing levels
The Jantsch Group reports that activation of the transcription factor MYC leads to an up-regulation of A-to-I editing, and that editing levels greatly differ between nascent pre-mRNA and mRNA in a cellular system, as well as in mouse tissues.
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GSE1 links the HDAC1/CoREST co-repressor complex to DNA damage.
The Seiser group discovered that genetic suppressor element 1 (GSE1) forms a complex with the HDAC1/CoREST deacetylase/demethylase co-repressor complex. While loss of GSE1 does not affect the histone deacetylation activity of CoREST, GSE1 appears to be essential for binding of the deubiquitinase USP22 to CoREST and for the deubiquitination of H2B K120 in response to DNA damage. The combination of deacetylase, demethylase, and deubiquitinase activity makes the USP22-GSE1-CoREST subcomplex a multi-enzymatic eraser that seems to play an important role during DDR.
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The Fgf/Erf/NCoR1/2 repressive axis controls trophoblast cell fate
The Latos group demonstrated that upon inhibition of the Fgf/Erk pathway in mouse trophoblast stem cells (TSCs), the Ets2 repressor factor (Erf) interacts with the Nuclear Receptor Co-Repressor Complex 1 and 2 (NCoR1/2) and recruits it to key trophoblast genes. Mechanistically, Erf regulates expression of these genes by recruiting the NCoR1/2 complex and decommissioning their H3K27ac-dependent enhancers.
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Proteins implicated in muscular dystrophy and cancer are functional constituents of the centrosome
The Winter and Bittner/Schmidt groups show that dystrophin, utrophin, dysferlin, and calpain-3 are functional constituents of the centrosome.
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A transition phase in late mouse oogenesis impacts DNA methylation of the early embryo
The Wossidlo/Arand group report on the nuclear rearrangements during the various transition stages of oocyte maturation, which are accompanied by changes in DNA methylation and Tet enzyme-catalyzed DNA modifications.
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