Changes in Retinal Chromatin Allow Animals To Be Nocturnal

Mariam Malik ‘22

Figure 1. Researchers at the University of Hiroshima discovered that nocturnal animals, such as lynxes, bats, and owls, are able to see at night because of changes in their retinal DNA. 

Night vision allows nocturnal animals to be active at nighttime and sleep when the sun is out, while diurnal animals are active during the day and sleep at night. However, when both diurnal and nocturnal animals are born, their ocular abilities are equal until a change in the cells of the eye occurs, allowing the animal to see in the dark. Through mathematics, Sungrim Seirin-Lee, Associate Professor, and Hiroshi Ochiai, lecturer at the University of Hiroshima in Japan, discovered that it is the chromatin’s structure in the cells of the eye that cause this change. 

First, the team of researchers observed the differences in nocturnal and diurnal mice, finding that there was a drastic difference in nuclear architecture around the retina between the two types. In nocturnal animals, DNA is in the middle of the nucleus. Heterochromatin, a type of DNA, usually remains on the nuclear envelope or on the roof of the nucleus. Lee and Ochiai, however, found that the heterochromatin can move if the nucleus changes shape. To further understand how the chromatin can move, researchers used a form of modeling called phase-field modeling. Scientists took numerous factors into account to formulate an equation, such as defining the free energy functions for the nucleus, chromosome territories, heterochromatin and chromocenters (CCs), and each composite’s individual volume. Another important aspect of the equation was to be able to manipulate the nuclear deformation, due to the fact that the nucleus deforming occurs independently of chromatin states. The team calculated the degree of deformation by the total area deviated from the circle divided by the area of the nucleus times 100. Furthermore, when observing heterochromatin in mice’s eyes, they discovered that conditional architecture caused deformation, which resulted in the inversion of the architecture of the nucleus. More specifically, two proteins are removed, allowing heterochromatin to move. 

To put their model to test, Seirin-Lee and Ochiai used neural stem cells, the most similar option to retinal cells. They treated cells with lamin B receptor (LBR) and lamins A/C (LamA/C), the proteins that keep heterochromatin on the nuclear envelope or at the top of the nucleus. Deformation of the nucleus stopped and a rise in chromatin clusters was seen, while nuclear architecture did not complete inversion. Both Seirin-Lee and Ochiai hope to conduct further research on if this revelation applies to all nocturnal mammals, and if there is even the possibility that humans could possess these structures by nuclear deformation. 



  1. S.S. Lee, et al., Role of dynamic nuclear deformation on genomic architecture reorganization. PLOS Computational Biology 15, 9 (2019). Doi: 10.1371/journal.pcbi.1007289
  2. Image received from:

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