10-Minute Presentation
Systematics, Evolution, and Biodiversity
Signe White (she/her/hers)
Postdoctoral Researcher
University of California
Berkeley, California
Elizabeth Gomez Cortez
Undergraduate Student
University of California, Berkeley
Berkeley, California
Michael Boots
Professor
University of California
Berkeley, California
When a host first encounters a pathogen, timing can determine whether infection takes hold or is stopped in its tracks. To examine how resistance unfolds through time, we tracked the expression of two immune genes—Gloverin and Hemolin—in Plodia interpunctella (Indian meal moth) larvae exposed to granulosis virus (PiGV). We compared two inbred populations that differ in viral resistance (IL-24, more resistant; IL-4, more susceptible) and sampled larvae at 0, 4, and 48 hours post-infection. Gene expression was quantified by qPCR, normalized to the housekeeping gene RpL32, and analyzed using the ΔΔCt method to estimate relative expression across treatments and time points.
The two genes revealed distinct temporal patterns. Gloverin, an early-acting antimicrobial peptide, was induced rapidly and strongly in the resistant IL-24 line but only weakly in the susceptible IL-4 line—suggesting that early activation contributes to effective viral control. Hemolin, a later-acting recognition and signaling molecule, showed the opposite trend: expression rose sharply at 48 hours in the susceptible line but remained moderate and regulated in the resistant one.
Together, these results show that resistance in P. interpunctella depends not only on immune strength but also on when key immune genes are activated. By following transcriptional responses through time, we reveal that the timing and regulation of gene expression may be just as important for viral resistance as the magnitude of the response itself.