Research Interests

Initially considered as “junk” DNA, it is now clear that the non-protein coding part of the human genome, which comprises about 98 % of the ~3·10⁹ DNA bases, is extensively transcribed and gives rise to numerous non-coding RNAs. In our group, we are mainly interested in deciphering the role of these RNAs in hematopoiesis and immune function. At the moment, we are focusing on two different types of non-coding RNAs, microRNAs (miRNAs) and long intergenic non-coding RNAs (lincRNAs).

MicroRNAs

MiRNAs are small, non-coding RNAs that mediate posttranscriptional silencing of a predicted 60% of protein-coding genes in mammals. In our work, we are trying to decipher how microRNAs influence early B lymphocyte development and, if aberrantly expressed, promote cellular transformation.

LincRNAs

LincRNAs form a heterogeneous group of long non-coding RNAs transcribed from independent genomic units that do not overlap with any coding genes. With few exceptions, we are far from understanding which of the thousands of lincRNAs expressed in each cell confers a regulatory function, and if so, how their function is mediated on the molecular level.

To unravel the role of individual lincRNAs in hematopoiesis and the immune system, we combine CRISPR/Cas9-mediated loss-of-function with a broad panel of molecular and biochemical approaches.

Recent Publications

An shRNA-mediated conditional knockdown of A1 protein in a mouse model highlights its role in B cell maintenance.

Conditional knockdown of BCL2A1 reveals rate-limiting roles in BCR-dependent B-cell survival

Solchalska, M., E. Ottina, S. Tuzlak, S. Herzog, M. Herold and A. Villunger

Cell Death Differ (2015); doi: 10.1038/cdd.2015.130

Here, we show that miR-125b triggers oncogenic transformation of B cell progenitors and identify MAP3K11, a regulator of mitogen- and stress-activated kinase signaling, as a critical target gene in this context.

MAP3K11 is a tumor suppressor targeted by the oncomiR miR-125b in early B cells.

Knackmuss, U., S.E. Lindner, T. Aneichyk, B. Kotkamp, Z. Knust, A. Villunger and S. Herzog

Cell Death Differ (2015); doi: 10.1038/cdd.2015.87

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