Simon Andrews

Simon Andrews did his first degree in Microbiology at the University of Warwick.  After a breif 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.

Latest Publications

TGFβ signalling is required to maintain pluripotency of human naïve pluripotent stem cells.
Osnato A, Brown S, Krueger C, Andrews S, Collier AJ, Nakanoh S, Quiroga Londoño M, Wesley BT, Muraro D, Brumm AS, Niakan KK, Vallier L, Ortmann D, Rugg-Gunn PJ

The signalling pathways that maintain primed human pluripotent stem cells (hPSCs) have been well characterised, revealing a critical role for TGFβ/Activin/Nodal signalling. In contrast, the signalling requirements of naive human pluripotency have not been fully established. Here, we demonstrate that TGFβ signalling is required to maintain naive hPSCs. The downstream effector proteins - SMAD2/3 - bind common sites in naive and primed hPSCs, including shared pluripotency genes. In naive hPSCs, SMAD2/3 additionally bind to active regulatory regions near to naive pluripotency genes. Inhibiting TGFβ signalling in naive hPSCs causes the downregulation of SMAD2/3-target genes and pluripotency exit. Single-cell analyses reveal that naive and primed hPSCs follow different transcriptional trajectories after inhibition of TGFβ signalling. Primed hPSCs differentiate into neuroectoderm cells, whereas naive hPSCs transition into trophectoderm. These results establish that there is a continuum for TGFβ pathway function in human pluripotency spanning a developmental window from naive to primed states.

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eLife, 10, 1, 31 08 2021

PMID: 34463252

Open Access

IL-7R signaling activates widespread V and D gene usage to drive antibody diversity in bone marrow B cells.
Baizan-Edge A, Stubbs BA, Stubbington MJT, Bolland DJ, Tabbada K, Andrews S, Corcoran AE

Generation of the primary antibody repertoire requires V(D)J recombination of hundreds of gene segments in the immunoglobulin heavy chain (Igh) locus. The role of interleukin-7 receptor (IL-7R) signaling in Igh recombination has been difficult to partition from its role in B cell survival and proliferation. With a detailed description of the Igh repertoire in murine IL-7Rα bone marrow B cells, we demonstrate that IL-7R signaling profoundly influences V gene selection during V-to-DJ recombination. We find skewing toward 3' V genes during de novo V-to-DJ recombination more severe than the fetal liver (FL) repertoire and uncover a role for IL-7R signaling in D-to-J recombination. Transcriptome and accessibility analyses suggest reduced expression of B lineage transcription factors (TFs) and targets and loss of D and V antisense transcription in IL-7Rα B cells. Thus, in addition to its roles in survival and proliferation, IL-7R signaling shapes the Igh repertoire by activating underpinning mechanisms.

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Cell reports, 36, 2, 13 Jul 2021

PMID: 34260907

Open Access

The global and promoter-centric 3D genome organization temporally resolved during a circadian cycle.
Furlan-Magaril M, Ando-Kuri M, Arzate-Mejía RG, Morf J, Cairns J, Román-Figueroa A, Tenorio-Hernández L, Poot-Hernández AC, Andrews S, Várnai C, Virk B, Wingett SW, Fraser P

Circadian gene expression is essential for organisms to adjust their physiology and anticipate daily changes in the environment. The molecular mechanisms controlling circadian gene transcription are still under investigation. In particular, how chromatin conformation at different genomic scales and regulatory elements impact rhythmic gene expression has been poorly characterized.

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Genome biology, 22, 1, 08 Jun 2021

PMID: 34099014

Open Access
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