An uninjured adult fruit fly pylorus – part of the gut that remains unchanged throughout the different life stages of the fly. Image credit: Cohen et al. (CC BY 4.0)
How does an injured organ replace cells that have died as a result of the damage? Making new cells might seem like the best option, because this would restore the organ to how it looked before the injury. To make new cells, existing cells in the organ divide. But not all organs make new cells to repair damage. Instead, some organs make their remaining cells bigger – a process known as hypertrophy – to fill the space created by the injury.
Cohen et al. have now developed a technique to investigate which method of repair a damaged organ uses. The technique uses genetic engineering to create an injury in a specific tissue in fruit flies, while also altering the activity of other genes that might affect how the tissue responds to the injury. Using the technique to study injuries to part of the gut that remains the same throughout a fly's life revealed that fly larvae repair this damage by creating new cells. However, adult flies repair the same injuries using hypertrophy.
Cohen et al. found that a gene known as ‘fizzy-related’ helps to control how the organ repairs damage. The fizzy-related gene produces a protein that stops cells dividing, which forces the cells to grow to repair any injuries to the organ. Adult flies that lacked the gene repaired their guts through cell division instead of by hypertrophy. This did not affect how well minor injuries to the gut were repaired. However, under conditions of more extreme tissue injury cell division distorted the gut and led to leakiness of gut contents.
Hypertrophy has been seen in injured human organs, including the heart, liver and kidneys. This was thought to be an abnormal response, but the results presented by Cohen et al. suggest that hypertrophy may instead help to protect the organs during repair. Further research into the role of hypertrophy could reveal ways to regenerate damaged organs, perhaps by targeting the activity of the fizzy-related gene.
