Dr Rhonda Taylor

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Research Associate

Dr Rhonda Taylor

Research Associate

Dr Rhonda Taylor


Profile

Dr Rhonda Taylor completed her bachelor of science with honours (genetics) at the University of Western Australia. In 2015, under the supervision of Dr Daniela Ulgiati, Rhonda completed her PhD which focussed on investigating the genetic association of the complement receptor two (CR2/CD21) gene with systemic lupus erythematosus (SLE). Her research primarily aimed to identify and characterise transcriptional regulatory mechanisms and the role of non-coding single nucleotide polymorphisms. Notably, Rhonda performed functional analysis of a single nucleotide polymorphism significantly associated with protection from SLE and located in intron one of CR2/CD21. She showed that the minor allele of this variant is associated with altered binding of the chromatin architecture protein CTCF leading to altered expression of the downstream gene, complement receptor one.

In 2015, Rhonda joined the Laing laboratory and is now applying her interest in regulation of gene expression to the field of muscle disease. Her current focus is characterising the transcriptional regulation of the alpha cardiac actin gene (Actc1) with the hope of upregulating the expression of Actc1 in post-natal skeletal muscle. This has significant potential as a therapeutic intervention for severe muscle disease caused by mutations in the alpha skeletal muscle actin (Acta1) gene. Further, this strategy, along with the power of gene-editing technologies, will also be applied to other muscle diseases for which an alternative gene isoform exists.

Dr Rhonda Taylor completed her bachelor of science with honours (genetics) at the University of Western Australia. In 2015, under the supervision of Dr Daniela Ulgiati, Rhonda completed her PhD which focussed on investigating the genetic association of the complement receptor two (CR2/CD21) gene with systemic lupus erythematosus (SLE). Her research primarily aimed to identify and characterise transcriptional regulatory mechanisms and the role of non-coding single nucleotide polymorphisms. Notably, Rhonda performed functional analysis of a single nucleotide polymorphism significantly associated with protection from SLE and located in intron one of CR2/CD21. She showed that the minor allele of this variant is associated with altered binding of the chromatin architecture protein CTCF leading to altered expression of the downstream gene, complement receptor one.

In 2015, Rhonda joined the Laing laboratory and is now applying her interest in regulation of gene expression to the field of muscle disease. Her current focus is characterising the transcriptional regulation of the alpha cardiac actin gene (Actc1) with the hope of upregulating the expression of Actc1 in post-natal skeletal muscle. This has significant potential as a therapeutic intervention for severe muscle disease caused by mutations in the alpha skeletal muscle actin (Acta1) gene. Further, this strategy, along with the power of gene-editing technologies, will also be applied to other muscle diseases for which an alternative gene isoform exists.

Research overview

  • Characterisation of transcriptional regulatory mechanisms in post-natal skeletal muscle
  • Upregulation of foetal gene isoforms as a therapy for muscle disease
  • CRISPR-Cas9 mediated gene editing and regulation of gene expression