Group leader


Dr. Asifa Akhtar

Senior Group Leader and Managing Director
Phone:+49 761 5108 565

Lab Asifa Akhtar

Assistant: Linda Schmidl phone: +49 761 5108 564 Email:

Selected Publications

Sarantis Chlamydas*, Herbert Holz*, Maria Samata*, Tomasz Chelmicki, Plamen Georgiev, Vicent Pelechano, Friederike Dündar, Pouria Dasmeh, Gerhard Mittler, Filipe Tavares Cadete, Fidel Ramírez, Thomas Conrad, Wu Wei, Sunil Raja, Thomas Manke, Nicholas M Luscombe, Lars M Steinmetz & Asifa Akhtar (2016)
Functional interplay between MSL1 and CDK7 controls RNA polymerase II Ser5 phosphorylation
Ramirez F*, Lingg T*, Toscano S*, Lam K*, Georgiev P, Chung H, Lajoie B, de Wit E, Zhan Y, de Laat W, Dekker J, Manke T, Akhtar A (2015)
High-Affinity Sites Form an Interaction Network to Facilitate Spreading of the MSL Complex across the X Chromosome in Drosophila
Meunier S *, Shvedunova M *, Van Nguyen N, Avila L, Vernos I and Akhtar A. (2015)
An epigenetic regulator emerges as microtubule minus-end binding and stabilizing factor in mitosis
Chelmicki T, Dündar F, Turley MJ, Khanam T, Aktas T, Ramírez F, Gendrel AV, Wright PR, Videm P, Backofen R, Heard E, Manke T, Akhtar A. (2014)
MOF-associated complexes ensure stem cell identity and Xist repression.
Dias J, Van Nguyen N, Georgiev P, Gaub A, Brettschneider J, Cusack S, Kadlec J, and Akhtar A. (2014)
Structural analysis of the KANSL1/WDR5/KANSL2 complex reveals that WDR5 is required for efficient assembly and chromatin targeting of the NSL complex.

Laboratory Asifa Akhtar

Laboratory Asifa Akhtar

DNA tightly packed together with histones into nucleosomes is not easily accessible to the enzymes that use it as a template for transcription or replication. Consequently, remodelling of chromatin structure plays an essential role in the regulation of gene expression. Structural changes in chromatin also form the basis for dosage compensation mechanisms that have evolved to equalise levels of X-linked gene products between males and females. In humans, one of the two X chromosomes in females is randomly inactivated by condensation of the chromosome into a Barr body, a process known as X-inactivation. In contrast, in Drosophila this is achieved by a two-fold hyper-transcription of the genes on the male X chromosome. Genetic studies have identified a number of factors that are important for dosage compensation in Drosophila, including five proteins [MSL1, MSL2, MSL3, MLE, MOF] and two non-coding RNAs [roX1 and roX2]. The hyperactive X is also specifically hyper-acetylated at histone H4, acetylation which is achieved by the MOF histone acetyl transferase.

The MSL complex in <em>Drosophila</em>, consisting of 2 non-coding RNAs and 5 proteins, is a key factor in male dosage compensation. Zoom Image
The MSL complex in Drosophila, consisting of 2 non-coding RNAs and 5 proteins, is a key factor in male dosage compensation. [less]

One of our major goals is to study the epigenetic mechanisms underlying X-chromosome specific gene regulation using Drosophila dosage compensation as a model system. More specifically, we are interested in addressing how the dosage compensation complex, composed of RNA and proteins [the MSL complex], gets targeted to the X chromosome. In addition, we are studying the mechanism by which the MSL complex modulates X chromosomal transcriptional output at a single cell resolution all the way to chromosomal and organismal level.

loading content