Using microarray technology to assess gene action, the researchers surveyed 84 genes that are turned on and 78 genes that are turned off as the fly embryo responds to wounding.
At all three time periods, the embryo's innate immune response kicked in, releasing the same types of antimicrobial peptides (short proteins) that an adult fly uses to fight infection. At 120 minutes, genes whose protein products repair the cuticle with new chitin, the meshwork composing the fly exoskeleton, respond. (The human version of this step, which may occur over several days, actually produces new cells because the cuts are larger.) Finally the fly embryo activates genes that color the cuticle.
The genes that aren't accessed as an embryo's wound heals are also telling. The fly cells at the wound site ignore genes involved in replicating DNA, maintaining chromosome structure, and cell growth and division. Overall, tracking the expression of the 162 genes revealed that the embryo temporarily halts development to repair the wound and keep infection at bay. Their findings made perfect sense; the organism concentrates its activities on addressing the immediate problem, healing the wound.
Like many biological processes, wound healing is fine-tuned. "A balance of gene activation and inhibition is required for efficient healing," said Dr. Juarez. Otherwise, a problem such as an ulcer, a chronic non-healing wound, or a thickening of the fly's cuticle can persist, she added.
The experiments revealed activities of eight genes that hadn't been suspected to participate in wound healing. These genes are expressed at very low levels or not at all in most cells, but are called into action when an injury breaks the cuticle.
Having identified these eight new genes that are activated in cells near puncture wounds in flies, researchers can now explore if genes in humans play comparable roles. "I t
|Contact: Phyllis Edelman|
Genetics Society of America