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John Roote

Researcher at University of Cambridge

Publications -  40
Citations -  4077

John Roote is an academic researcher from University of Cambridge. The author has contributed to research in topics: Drosophila melanogaster & Gene. The author has an hindex of 26, co-authored 40 publications receiving 3841 citations.

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In Vivo Analysis of Proteomes and Interactomes Using Parallel Affinity Capture (iPAC) Coupled to Mass Spectrometry

TL;DR: In this article, a pipeline for determining interactomes by Parallel Affinity Capture (iPAC) is described and used by identifying partners of several protein baits with a range of sizes and subcellular locations.
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Distinct functions of Mst77F and protamines in nuclear shaping and chromatin condensation during Drosophila spermiogenesis

TL;DR: Data support the long-standing hypothesis that the switch from a histone- to protamine-based chromatin protects the paternal genome from mutagens.
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The multiple wing hairs gene encodes a novel GBD-FH3 domain containing protein that functions both prior to and after wing hair initiation

TL;DR: The authors' data argued early proximal Mwh accumulation restricts hair initiation to the distal side of wing cells and the later hair accumulation of Mwh prevents the formation of ectopic secondary hairs, which appears to be a feedback mechanism that limits cytoskeleton activation to ensure a single hair is formed.
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The genetics of a small autosomal region of Drosophila melanogaster containing the structural gene for alcohol dehydrogenase. VII. Characterization of the region around the snail and cactus loci.

TL;DR: The genetic interval 35C to 36A on chromosome arm 2L of Drosophila melanogaster has been saturated for mutations with visible or lethal phenotypes, and 38 loci have been characterized, including several maternal-effect lethals and several early embryonic lethals, including snail and fizzy.
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The tamas gene, identified as a mutation that disrupts larval behavior in Drosophila melanogaster, codes for the mitochondrial DNA polymerase catalytic subunit (DNApol-gamma125).

TL;DR: It is determined that the lack of response to light in these mutants was due to a primary deficit in locomotion and was renamed tamas (translated from Sanskrit as "dark inertia").