Just Accepted Papers

  • Deryas‘ paper titled ” Cryptochrome deletion in p53 mutant mice enhances apoptotic and anti-tumorigenic responses to UV damage at the transcriptome level” was accepted to be published in Functional & Integrative Genomics

This paper describes new pathways contribute apoptosis in p53Cry1Cry2 triple  knockout mouse.

  • Handes’ paper titled ” Comparative RNA-seq analysis of the drought sensitive lentil (Lens culinaris) root and leaf under short- and long-term water deficits” was accepted to be published in Functional & Integrative Genomics.

This paper describes how duration of the drought stress hits the circadian rhythm and other pathways in lentil.

  • Denizspaper from Karalar Group titled “Centriolar satellites are required for efficient ciliogenesis and ciliary content regulation” was accepted to be published in EMBO Reports.


Circadian Clock

Our laboratory is interested in understanding how clock works at cellular level. For more information please visit our research interest section. 

Almost every day, we wake up, get hungry, feel ourselves energetic or tired or succumb to sleep at the same hours. Although people may have different cycles, at certain hours of the day our bodies show the same responses. The circadian clock regulates the timing of sleep and wakefulness and, therefore, all dependent behavioural and physiological processes. In humans, a defect in the clock gene PER2 produces familial advanced sleep phase syndrome (FASPS); an analogous mutation causes the same phenotype in mice. People with a causal mutation in casein kinase CSNK1D and an associated variant in CSNK1E display ASPS and delayed sleep phase syndrome (DSPS), respectively. Finally, a human CLOCK variant is associated with diurnal sleep preference. Circadian clock genes are also associated with a host of neurological disorders including schizophrenia, unipolar major depression, and bipolar disorder.  Although it was widely believed that circadian clock disruption predisposes humans to cancer based largely on epidemiologic data, studies with Cry mutant mice revealed a more complex pattern of interactions among the clock, apoptosis, and oncogenic transformation.