Líffræðifélag Íslands
Líffræðiráðstefnan 2015
Erindi/veggspjald / Talk/poster E101
Ehsan Pashay Ahi (1), Samantha V. Beck (2), Camille Leblanc (2), Bjarni K. Kristjánsson (2), Zophonías O. Jónsson (1,3)
1.Institute of Life and Environmental Sciences, University of Iceland, Sturlugata 7, 101 Reykjavik, Iceland, 2. Holar University College, Saudarkrokur, Iceland, 3. Biomedical Center, University of Iceland, Vatnsmýrarvegur 16, 101 Reykjavik, Iceland.
Kynnir / Presenter: Zophonías O. Jónsson
Tengiliður / Corresponding author: Zophonías O. Jónsson (zjons@hi.is)
Egg size is an indicator of female energetic investment in reproduction and variation in egg size can directly affect offspring survival. The effects of variable egg size on offspring survival can be exerted through compensatory mechanisms involved in early growth. There is increasing evidence that egg size can be adjusted by mothers in response to different physiological and environmental conditions such as nutritional status and stress levels. The molecular mechanisms underlying the production of eggs with variable sizes are poorly understood. Also, the potential links between molecular mechanisms influencing egg size and the molecular pathways involved in early developmental patterning and growth are still not well characterized. Recently, we have identified a component of the glucocorticoid signaling pathway, Sgk1, displaying higher levels of maternal transcripts in larger eggs of an Icelandic Arctic charr morph with highly variable egg size. In this study, we investigated molecular mechanisms that could underpin the association between Sgk1 maternal transcript levels and the variation of egg size across three contrasting Arctic charr morphs in Iceland. We used an iterative expression profiling approach on candidate genes which were selected based on Sgk1-related co-expression data from vertebrate model species. After identification of conserved networks of co-expressed genes showing expression correlation with variation in egg size between the morphs, we also found c-Jun, a component of Ap-1 transcription factor, to be a potential upstream regulator of the networks.