Research
How does the most dynamic part of our DNA shape who we are, what we eat, and what makes us sick?
My work sits at the intersection of evolutionary genetics, genomics, and glycoproteomics — four threads, one question.
01 · MUCINS Explore →
Mucins
How evolution builds the slippery, sugar-coated proteins that make mucus.
→ Identified the secretory calcium-binding phosphoprotein (SCPP) locus as a hotspot for de novo mucin evolution in mammals.
→ Documented 27 previously undescribed mucins, with 15 independent instances of mucin evolution.
→ Confirmed expression of a subset of these mucins in saliva by gel electrophoresis and mass spectrometry.
02 · SALIVA Explore →
Saliva
The mouth's first line of defense as a window into dietary adaptation.
→ Documented amylase (AMY) gene copy-number expansions that arose independently in multiple starch-eating mammals.
→ Provided correlative evidence that AMY duplication may be a first step for amylase to be expressed in saliva.
→ Traced the likely mechanism of independent AMY duplication to retrotransposon events.
03 · TRADEOFFS Explore →
Evolutionary Tradeoffs
Why evolution keeps disease-linked genetic variants around.
→ A common 32 kb deletion of LCE3B/LCE3C (associated with psoriasis) is ancient, predating the Human–Denisovan divergence.
→ The haplotype shows high allele frequency, elevated nucleotide diversity, excess intermediate-frequency variants, and unusually deep coalescence.
→ Results are most consistent with the deletion being maintained by balancing selection in humans.
04 · GLYCOPROTEOMICS Explore →
Glycoproteomics
Reading the sugar code on proteins to understand function and disease.
→ PLACEHOLDER — add key results as the Yale/Malaker work develops.
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