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Morrill, L.

Publications and source records attributed to Morrill, L..

2 recordsLinked to original sources

Genetic encoding of 3-cyano-tyrosine and its use in controlling the chromophore isomeric state of the fluorescent protein mKate

Switchable {beta}-barrel-type fluorescent proteins are essential genetically encoded probes for super-resolution imaging. The space required for chromophore cis-trans isomerisation can also provide an opportunity to introduce bulkier chemistry at the 3-position of the phenolic ring. Here, we report, to our knowledge, the first successful genetic encoding of 3-cyano-L-tyrosine (3CNY) into a protein. Using genetic code expansion, the cyano-containing amino acid was incorporated directly into the chromophore of mKate, a pH-dependent switchable red fluorescent protein. In mKate, the chromophore adopts a fluorescent phenolate cis state at physiological pH, transitioning to a phenolic trans state under acidic conditions. Substitution of the native tyrosine with 3CNY yields a functional protein exhibiting hypsochromically shifted spectral properties. Time-dependent density functional theory (TD-DFT) calculations indicate that 3CNY incorporation results in a trans state at pH 8. Unlike mKate, the trans state is fluorescent. In contrast, incorporation of 3-chloro-L-tyrosine (3ClY) preserves the preference for the cis phenolate state. Molecular modelling suggests that the cyano group can form stabilising hydrogen bonds with residues S143 and S158, promoting the trans configuration. DFT analysis further indicates that the electron-withdrawing cyano group perturbs conjugation across the chromophore, potentially lowering the barrier to cis-trans isomerisation. Conversely, wild-type and 3ClY variants maintain polarised HOMO and LUMO distributions in the cis state, supporting stronger conjugation and a reduced HOMO-LUMO gap. Overall, the introduction of a genetically encoded 3-CNY tyrosine analogue into a fluorescent protein chromophore expands our mechanistic understanding and enables incorporation of a new chemical tag directly into the chromophore.

biochemistry↗

The genomic landscape of early stage ovarian high grade serous carcinoma

PurposeHigh grade serous carcinoma (HGSC) is the commonest type of ovarian cancer. Nearly all HGSC cases are diagnosed at late stage and it is not clear whether early stage HGSC has unique characteristics compared to late stage tumours. Experimental DesignWe analysed samples from 45 patients with FIGO stage I - IIA HGSC - 40 from the pathology archives of three large UK cancer centres and 5 from the BriTROC-1 study. We performed shallow whole genome sequencing (sWGS) and targeted next generation sequencing to investigate somatic mutations and copy number alterations. We compared results to 51 stage IIIC/IV HGSC patients from the BriTROC-1 study. ResultsThere was no difference in median age between the early stage (median 61.3 years, range 40-84) and late stage (median 62.3 years, range 34-76) patients at diagnosis. TP53 mutations were near-universal (92% early stage, 100% late stage samples) and there were no significant differences in the rates of other somatic mutations, including BRCA1 and BRCA2, or focal copy number alterations between early- and late-stage cohorts. There were also no unique amplifications or deletions in either cohort. However, median ploidy was greater in late stage (median 3.1) than early stage (median 2.0) samples. In addition, there were higher numbers of breakpoints per 10MB and per chromosome arm and higher absolute copy number in late stage than early stage cohorts; early stage samples had longer segment length. Overall copy number signature exposures were significantly different between early and late stage samples with greater signature 3 exposure in early stage and greater signature 4 in late stage. Both simplex plot and unsupervised hierarchical clustering suggested that a subset of late stage samples retain early stage appearances with high signature 3 and co-clustering with the early stage samples ConclusionsThese data suggest that there are no unique mutations or focal copy number alterations in early stage HGSC. However, whole genome duplication is significantly more common in late-stage disease, suggesting evolution during disease progression. However, a subset of late stage HGSC retains early-stage features, which are associated with improved overall survival.

cancer biology↗