Cell Division Cycle 48 (CDC48; also known as p97/Vasolin-containing protein, VCP) is one of the most abundant proteins in eukaryotic cells, accounting for 1% of cytosolic proteins (Baek et al., 2013). It is a highly-conserved AAA+ ATPase chaperone that utilizes the energy of ATP hydrolysis to pull, extract, and unfold ubiquitylated or sumoylated proteins associated with soluble or membrane-associated protein complexes involved in a variety of essential cellular functions including: 1) cell cycle regulation, 2) endoplasmic reticulum-associated degradation (ERAD), 3) membrane biogenesis,4) protein turnover via the ubiquitin-proteasome pathway, 5) autophagosome biogenesis and 6) maintenance of DNA integrity (Woodman, 2003; Meyer et al., 2002; Hoppe et al., 2000). In Arabidopsis thaliana, there are three genes encoding CDC48 isoforms, AtCDC48a, AtCDC48b, and AtCDC48c (Rancour et al., 2004). Disruption of AtCDC48a, results in pleiotropic developmental defects in embryogenesis, seedling growth, and pollen tube growth likely through its activity in regulating cell division and elongation (Park et al., 2008). The Arabidopsis PUX1 protein regulates CDC48 function in plant growth and cell elongation. Rather than functioning as a cofactor, PUX1 inactivates the ATPase activity and promotes the disassembly of the homohexameric CDC48/p97 complex (Park et al., 2004).
Interestingly, loss of PUX1, a negative regulator of CDC48 activity, results in enhanced growth phenotypes in the pux1 mutants (Rancour et al., 2004). These phenotypes are similar to GA-induced root and shoot growth. Additionally, preliminary data from our lab have indicate that PUX1 functions as a negative regulator of GA-dependent processes during plant growth and development, including shoot and root growth, seed germination, and the transition to flowering. Our lab is currently further investigating the molecular mechanism underlying PUX1 regulation of GA signaling via its interaction with its GA receptor, GID1, and CDC48A to control plant growth and development.