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Siddiqui, K. S.

Publications and source records attributed to Siddiqui, K. S..

2 recordsLinked to original sources

To FRET or Not to FRET: Bioinformatics and Fluorescence Spectroscopy suggest that Reduced Tryptophan to Heme Energy Transfer Facilitates Lignin Degradation in Class II Peroxidases

A key step in the evolution of lignin-degrading enzymes is revealed by the observation that, unlike other heme-proteins studied to date, Class II peroxidases exhibit minimal energy transfer from tryptophan (Trp) to heme residues. Bioinformatics analyses and molecular dynamics simulations of Class II (MnP and VP) and Class III (horseradish peroxidase, HrP) structures indicate that the Trp residue in HrP has the highest orientational factor and fluorescence resonance energy transfer (FRET) efficiency. By contrast, Trp residues in MnP and VP display low FRET efficiency due to unfavorable orientation factors despite their proximity to the heme. Steady-state fluorescence experiments confirmed this low FRET efficiency, showing strong emission in MnP and VP but weak emission in HrP. This decreased Trp-to-heme energy transfer appears to minimize competition between direct FRET and long-range electron transfer (LRET), allowing electrons to flow from bulky lignin substrates to the heme center. Such a mechanism likely provided a selective advantage during the evolution of Class II peroxidases, facilitating efficient lignin degradation at the enzyme surface. HighlightsClass II peroxidases show reduced Trp-to-heme FRET compared with HRP MD simulations reveal unfavorable Trp-heme orientation in VP and MnP Low FRET correlates with strong Trp fluorescence in VP and MnP Reduced FRET favors long-range electron transfer (LRET) during lignin oxidation Findings suggest an evolutionary adaptation in lignin-degrading peroxidases O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=128 SRC="FIGDIR/small/697144v1_ufig1.gif" ALT="Figure 1000"> View larger version (36K): org.highwire.dtl.DTLVardef@f8b3a8org.highwire.dtl.DTLVardef@1db18a4org.highwire.dtl.DTLVardef@12ebf1dorg.highwire.dtl.DTLVardef@54712_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

Unveiling the evolutionary code of NOTCH3: mammalian bioinformatics sheds light on human pathogenicity.

NOTCH3 is a highly conserved transmembrane receptor implicated in CADASIL, a hereditary small vessel disease driven by mutations in its extracellular EGF-like repeats. The mechanism by which these mutations cause pathology remains unclear. We present the first large-scale comparative bioinformatic analysis of NOTCH3 across 113 mammalian species, uncovering three novel insights: i) a remarkable evolutionary conservation of all 204 cysteines, with the only exception being eight naturally occurring cysteine mutations in jaguar (EGFr13-15); ii) a unique deletion in Brandts bat regulatory region, which may expose it to proteases, potentially altering signaling; iii) a rare human NOTCH3-X1 isoform, absent in most mammals but shared with select primates, a bat, and elephants, involving a cysteine-depleting deletion spanning EGFr20-22. These features provide novel evolutionary insights into human pathogenicity and suggest testable targets for in vivo experiments. Our study highlights the potential of comparative bioinformatics to identify previously hidden functional elements in disease-associated mammalian proteins. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=107 SRC="FIGDIR/small/678708v2_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@5b54cforg.highwire.dtl.DTLVardef@1d0725org.highwire.dtl.DTLVardef@1c0417corg.highwire.dtl.DTLVardef@10b4b5b_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioinformatics↗