Investigating the Role of N-linked Glycosylation-Associated, Mid-gestation Lethal Knockout Mouse Lines in Placental Development

Presenter

Rossella Marina Gargiulo

Campus

UMass Amherst

Sponsor

Kimberly D. Tremblay, Department of Animal Sciences, UMass Amherst

Schedule

Session 4, 2:30 PM - 3:15 PM [Schedule by Time][Poster Grid for Time/Location]

Location

Poster Board A35, Campus Center Auditorium, Row 2 (A21-A40) [Poster Location Map]

Abstract

The placenta is the support organ that connects the embryo to the mother during gestation and is required for proper development. We find that loss of Asparagine-linked glycosylation 3 (Alg3) or Subunit of oligosaccharyltransferase complex (Stt3b) result in midgestation lethality and placentation defects. Both genes are in the N-linked glycosylation pathway, which is necessary for proper folding and function of proteins in the secretory pathway. To promote embryonic development, a major role of the placenta is the secretion of proteins such as hormones, growth factors, and cytokines. Therefore we hypothesize that the placenta is susceptible to disruptions in N-linked glycosylation. To examine the role for N-linked glycosylation during placentation, I aim to analyze the quantity and distribution of N-linked glycoproteins in Alg3 and Stt3b null and control placentas. Using periodic acid-Schiff (PAS) staining, a general polysaccharide stain, I did not find discernible distinctions between Alg3 and Stt3b null and control placentas. I will continue analysis by performing lectin staining to identify specific N-linked glycans. In addition, N-linked glycosylation is required for proper folding of secretory proteins in the endoplasmic reticulum (ER). We hypothesize there will be increased ER stress and activation of the unfolded protein response (UPR) that could lead to the observed defects in Alg3 or Stt3b null placentas. We will perform RT-PCR on Alg3 and Stt3b null and control placentas to look for the activation and upregulation of ER stress markers and UPR genes. These analyses will help to elucidate the role of Alg3 and Stt3b during gestation.

Keywords

Placental defects, Glycosylation, Embryonic development, Endoplasmic reticulum stress, Mouse

Research Area

Biological Organisms

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