Charles J. Weitz is a chronobiologist and neurobiologist whose work primarily focuses on studying the molecular biology and genetics of circadian clocks.
At Harvard University, the Weitz lab consolidated understanding towards the transcriptional architecture of the circadian clock in Drosophila and mice models.
[1] The Weitz lab is also accredited for discovering direct transcription termination by the PER complex, which regulates the expression of genes involved in producing the circadian rhythm.
[8] In Drosophila, CRY functions as a circadian photoreceptor by binding to TIM and inhibiting the PER-TIM negative feedback loop in response to light.
Weitz, Griffin Jr., and Staknis investigated this hypothesis in 1999 and discovered that the two CRY homologs, CRY1 and CRY2, negatively regulate Per1 transcription by inhibiting the CLOCK-BMAL1 complex, independent of light.
This results of Weitz’s study allowed them to conclude Per1 plays an important role in peripheral and output pathways of the circadian clock.
[13] As the PER complex is produced, the SETX interacts with the accumulated RNA polymerase II, blocking its release and inhibiting further transcription of the PER and CRY genes.
[13] This discovery solidified insight into how PER proteins may repress clock-controlled target genes directly, contributing to future studies of the circadian clock's transcriptional architecture.
[12] Cryo-electron microscopy (cryo-EM) is a cutting-edge technique that determines the three-dimensional structure of large molecules at high resolution.
[14] In 2017, Weitz, alongside Rajindra Aryal, Pieter Bas Kwak, Alfred Tamayo and Michael Gebert, applied this technique to enrich the understanding of the mammalian circadian clock.
[15] In a 2008 paper, Katja A. Lamia, Kai-Florian Storch along with Charles Weitz discovered that a liver specific mutation to the Bmal1 gene results in low glucose levels during the fasting period of the mices’ feeding cycle.