Submission Date

7-18-2024

Document Type

Paper- Restricted to Campus Access

Department

Biology

Faculty Mentor

Rebecca Lyczak

Comments

Presented during the 26th Annual Summer Fellows Symposium, July 19, 2024 at Ursinus College.

Research funded by NIH grant 2R15GM110614-03

Project Description

Caenorhabditis elegans is a transparent nematode ideal for studying early embryonic mechanisms such as mitosis and meiosis. Mitosis is an important process involving the division of cells, and the spindles in mitosis are necessary for the separation of chromosomes. The centrosomes of mitosis are important for the organization of these spindles. When these processes go wrong, additional problems like cancer may arise. The pam-1 gene encodes for a puromycin-sensitive aminopeptidase (PAM-1) in C. elegans. In mitosis, pam-1 mutant embryos are more likely to divide symmetrically rather than asymmetrically. PAM-1 is required to prevent premature centrosome movements and to properly attach the chromosomes to the mitotic spindle. Furthermore, the absence of PAM-1 triggers the spindle assembly checkpoint. The proteins β-tubulin, SPD-2, and SPD-5 are all important proteins for the spindle structures of C. elegans. I will be looking at the mitotic spindles through these proteins marked with GFP and RFP and trying to understand how the pam-1 mutation affects spindle assembly, more specifically relating to the timing of spindle assembly and the overall structure of the centrosome. To study this, wildtype and pam-1 mutant C. elegans spindle structures will be looked at during the first mitosis using the confocal microscope. So far, it has been seen that the pam-1 mutant embryos have centrosomes that move prematurely and larger sperm asters than the wildtype C. elegans. This research is done with hopes of discovering more about the mitotic spindles in the pam-1 mutant embryos of C. elegans.

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