TY  - GEN
T1  - Characterizing Dynein’s Role in P-cell Nuclear Migration using an Auxin-Induced Degradation System
AU  - Ho, Jamie
AU  - Valdez, Venecia A.
AU  - Ma, Linda
AU  - Starr, Daniel A.
DO  - 10.17912/W2W96J
UR  - http://beta.micropublication.org/journals/biology/w2w96j/
AB  - Nuclear migration limits the rate of cellular migration through narrow spaces due to the large size and stiffness of the nucleus (Ungricht and Kutay, 2017). Using Caenorhabditis elegans as a model organism, we can observe P-cell nuclear migration in vivo. During the mid-L1 stage, P-cell nuclei that are about 3-4μm in diameter must migrate from a lateral to ventral position. This migration occurs through a constricted space ~ 200nm wide, about 5% of the diameter of the relaxed nucleus, between body wall muscle and cuticle (Cox and Hardin, 2004). If this migration succeeds, P-cells develop into vulval cells and GABA neurons. Failure of P-cell nuclear migration leads to cell death and missing P-cell lineages, leading to egg laying defective (Egl) and uncoordinated (Unc) animals because of missing vulval cells and GABA neurons, respectively (Sulston and Horvitz, 1981). Two proteins that are known to be involved in P-cell nuclear migration are UNC-84 and UNC-83. These proteins make up the LINC complex to form a bridge between the nucleus and the cytoplasm. Disruption of the LINC complex leads to nuclear migration defects in P-cells (Starr et al., 2001). Previously, our lab showed that P-cell nuclei migrate towards the minus ends of microtubules through the microtubule motor, dynein. Dynein is essential in embryogenesis (Gonczy et al., 1999), therefore our research was previously limited to viable, partial loss-of-function alleles of dynein or dynein-interacting proteins. Animals expressing a hypomorphic allele of dynein, dhc-1(js319), had an average of ~3 P-cells that failed to migrate (Bone et al., 2016).
PY  - 2018
JO  - microPublication Biology
ER  -