Sudarshan Pinglay

The paper introduces OPTIMuS PRIME-Del, a CRISPR-based method for multiplexed, precise deletion of cis-regulatory elements, validated through molecular tagging and scRNA-seq analysis.

This paper introduces Shred-seq, a method to scan large-scale deletions in the human genome, revealing essential regions including noncoding sequences and establishing a lower bound for viability.

The paper introduces an improved plasmid toolkit to streamline the mSwAP-In method for large-scale genome writing in mammalian cells.

The paper develops iPSC-SGE to assess variant effects in diverse genetic and cell contexts, identifying pathogenic variants and essential disease genes.

This paper introduces SGE, a method for screening metabolic pathways in mammalian cells, and finds that mitochondrial localization and large synthetic DNA constructs are key for successful pathway engineering.

This paper introduces Genome-Shuffle-seq, a method for generating and mapping structural variants in mammalian genomes, and demonstrates its application in mouse embryonic stem cells.

The paper designs and characterizes diverse genomic parts for precise genome editing and molecular recording in mammalian cells.

This paper demonstrates the successful restoration of valine biosynthesis in mammalian cells by integrating synthetic pathways from E. coli, showing that ancient metabolic pathways can be reactivated in metazoans.

MenDEL automates the selection of BAC sets to cover long DNA regions by allowing users to define criteria and find optimal combinations from existing libraries.

The paper uses synthetic genomic reconstitution to study Hox cluster regulation, finding that distal enhancers are required for full transcriptional output while chromatin remodeling can occur without them.

The paper describes a pipeline for de novo assembly, delivery, and expression of a 101 kb human gene in mouse cells, demonstrating functional evaluation of a full-length gene.

The paper uses ancestral resurrection to show that changes in the β3-C loop and gatekeeper residue in ERK kinases drove the evolution of lower intrinsic autophosphorylation.