Meeting Abstract
Holometabolous insects have been able to radiate and capture numerous ecological niches due to the appearance of unique appendages in the adults compared to the larvae. All appendages, such as the wings, and antennae, begin as clusters of undifferentiated cells called imaginal discs that propagate at the last larval instar. Inability to repair damage to imaginal discs could compromise body scaling; hence impairing their ability to radiate to required geographical niches. Delaying development has risen as a mechanism to combat this issue by giving damaged tissues enough time to regenerate. Damage to the imaginal discs of the hornworm, Manduca sexta, using X-ray radiation, results in delays to pupation and metamorphosis. It remains unclear how damaged imaginal discs signal the rest of the body to delay development, allowing them to recuperate from the damage. Interestingly, damaged larvae show increased critical weight, which suggests extended synthesis or slow degradation of the developmental hormone, Juvenile Hormone (JH), plays a role. Therefore, I hypothesized that damaged imaginal discs coordinate developmental delays through the actions of JH; thus, the decrease of JH downstream transcription factor kruppel homolog 1 (kr-h1) would be delayed in larvae damaged by x-ray radiation. I verified this by measuring changes kr-h1 using qRT-PCR. This study can be confirmed using JH agonists and antagonists in larvae lacking the JH-producing glands. Defining JH as a modulator of damage-induced delays could establish a novel mechanism to cope with tissue damage in holometabolous insects. In addition, it will establish a simpler insect model for studying body allometry when tissues are developing more slowly due to healing or regeneration after tissue damage.
