DNA damage: offing KAP to stay focused in the dark.
To optimize night vision, nocturnal mammals exploit the light refractive properties of heterochromatin, adopting a unique nuclear structure that positions heterochromatin at the center of the nucleus focusing light on photoreceptors. This strategy comes at the expense of genome protection because DNA breaks cannot be repaired in dense heterochromatin.
Department of Small Animal Clinical Sciences, Michigan State University, East Lansing, MI 48823, USA; College of Veterinary Medicine, Michigan State University, East Lansing, MI 48823, USA.
Simon
S
Petersen-Jones
Department of Microbiology and Molecular Genetics, and Department of Pathobiology and Diagnostic Investigation, Michigan State University, East Lansing, MI 48823, USA; College of Veterinary Medicine, Michigan State University, East Lansing, MI 48823, USA. Electronic address: kmeek@msu.edu.
Katheryn
K
Meek
D000818:Animals; D064007:Ataxia Telangiectasia Mutated Proteins / Q000235:genetics; D053903:DNA Breaks, Double-Stranded; D004260:DNA Repair; D004268:DNA-Binding Proteins; D063146:Polycomb-Group Proteins; D017948:Retinal Rod Photoreceptor Cells / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics*
D004268:DNA-Binding Proteins; C533390:Phf1 protein, mouse; D063146:Polycomb-Group Proteins; D014157:Transcription Factors; D064007:Ataxia Telangiectasia Mutated Proteins; C576325:Atm protein, mouse