Simon Andrews

Simon Andrews
Simon Andrews
Simon Andrews
Head of Bioinformatics Facility
Simon Andrews

Simon Andrews did his first degree in Microbiology at the University of Warwick.  After a brief period working for Sandoz pharmaceuticals he went on  to do a PhD in protein engineering a the University of Newcastle with Harry Gilbert.  During his PhD his interests moved from bench work toward the emerging field of bioinformatics, and he decided to follow this direction in his future career.

After completing his PhD Simon worked with the BBSRC IT Services where he developed and then presented a series of bioinformatics training courses in protein structure analysis to the BBSRC institutes.  At one of these courses at Babraham he met John Coadwell who establised the Babraham Bioinformatics group and was then employed as the second member of the bioinformatics team.  Since joining Babraham Simon has seen the group grow from two people to nine as the field has become far more prominent in the biological research community.  He took over the running of the group in 2010. Simon won a Papin Prize in 2025 for contributions to research (news article link).

Latest Publications

Cockayne L, Conroy MJ, Baloglu C, Fahy E, Hagn G, Quehenberger O, Armando AM, Lombardi Bendoula G, Galano JM, Sánchez-Illana Á, Durand T, Kampschulte N, Kennedy PD, Gijón M, Tsugawa H, Arita M, Maxey K, Truskowski M, Kuda O, Khan S, Homer NZM, Matsuzawa Y, Domingues R, Meikle PJ, Giles C, Huynh K, Murphy RC, Wang Z, Xia Y, Guan XL, Ekroos K, Liebisch G, Merrill AH, Lopez-Clavijo AF, Campopiano D, Wheelock CE, Subramaniam S, Andrews R, Goracci L, Ni Z, Fedorova M, Andrews S, Griffiths W, Andrew R, Dennis EA, O'Donnell VB Bioinformatics

As lipidomics approaches its 25th anniversary, we explore how lipid research has matured over the years while highlighting emerging innovations that are expanding our ability to study these diverse, life-critical biomolecules. In particular, we showcase the community-driven, open-access databases, software, and educational resources made freely available through the ELIXIR Core Data Resource LIPID MAPS for the benefit of both established and new researchers.

+view abstract Science signaling, PMID: 42085532

Kara N, Biggins L, Whale A, May K, Grinkevich V, Garran-Garcia P, Srinivasan J, Rugg-Gunn PJ, de Almeida CR, Walker SJ, Picco G, Garnett MJ, Andrews S, Parry A, Robinson HMR, Houseley J Epigenetics , Genomics , Biological Support Unit , Bioinformatics

TrAEL-seq is a robust method for profiling DNA replication genome-wide that works in unsynchronized cells and does not require drugs or nucleotide analogues. Here, we provide an updated method for TrAEL-seq that improves sample quality and includes multiplexing of up to six samples which dramatically improves throughput, and we validate TrAEL-seq in multiple mammalian cell lines. The updated protocol is straightforward and robust yet provides excellent resolution comparable to OK-seq in mammalian cell samples. High resolution replication profiles can be obtained across large panels of samples and in dynamic systems, for example during the progressive onset of oncogene induced senescence. In addition to mapping zones where replication initiates and terminates, TrAEL-seq is sensitive to replication fork speed, revealing effects of both transcription and proximity to replication Initiation Zones on fork progression. Although forks move more slowly through transcribed regions, this does not have a significant impact on the broader dynamics of replication fork progression, and instead replication forks accelerate across the first ∼1 Mb of travel irrespective of local transcriptional activity. We propose that this is a consequence of fewer replication forks being active later in S-phase when these distal regions replicate and there being less competition for replication factors.

+view abstract Nucleic acids research, PMID: 41830325

White HN, Chovanec P, Biggins L, French EC, Bullen G, Andrews S, Corcoran AE Epigenetics , Bioinformatics

The diversity of antibodies underpins robust immune responses. During the formation of the antibody repertoire in early bone marrow B-cells, random antibody heavy-chain proteins are generated from recombined VH, DH, and JH gene segments. Many are non-functional and are negatively selected. To understand this process in normal mice, we have undertaken an in-depth analysis of heavy-chain selection at this pre-B cell transition. We find independent selection acting on three regions of the complementarity-determining region 3 (CDR3) antigen-binding site, with particularly heavy counter-selection against certain productive VH/JH combinations. This led us to hypothesise that VH-replacement, where the VH gene segment in an existing VDJ combination is replaced, targets productive VDJ rearrangements that code for non-functional heavy chains. We detect VH-replacement recombination products that closely follow the pattern of selection of functional and non-functional VDJ rearrangements. This reveals a physiological role for VH-replacement in the developmental release of B-cells that are stalled by non-functional heavy-chains. This leads to re-modelling of the restricted early VDJ repertoire toward the use of other VH gene segments throughout the IgH locus.

+view abstract The EMBO journal, PMID: 40913135

Group Members

Simon Andrews

Head of Bioinformatics Facility

Chetin Baloglu

LIPID MAPS Web Developer

Laura Biggins

Core Bioinformatician

Hayley Carr

Biological Statistician

Sarah Inglesfield

Core Bioinformatician

Jo Montgomery

Scientific Training and Data Integrity Manager