Arabidopsis COG Complex Subunits COG3 and COG8 Modulate Golgi Morphology, Vesicle Trafficking Homeostasis and Are Essential for Pollen Tube Growth

Abstract

Spatially and temporally regulated membrane trafficking events incorporate membrane and cell wall materials into the pollen tube apex and are believed to underlie the rapid pollen tube growth. In plants, the molecular mechanisms and physiological functions of intra-Golgi transport and Golgi integrity maintenance remain largely unclear. The conserved oligomeric Golgi (COG) complex has been implicated in tethering of retrograde intra-Golgi vesicles in yeast and mammalian cells. Using genetic and cytologic approaches, we demonstrate that T-DNA insertions in Arabidopsis COG complex subunits, COG3 and COG8, cause an absolute, male-specific transmission defect that can be complemented by expression of COG3 and COG8 from the LAT52 pollen promoter, respectively. No obvious abnormalities in the microgametogenesis of the two mutants are observed, but in vitro and in vivo pollen tube growth are defective. COG3 or COG8 proteins fused to green fluorescent protein (GFP) label the Golgi apparatus. In pollen of both mutants, Golgi bodies exhibit altered morphology. Moreover, γ-COP and EMP12 proteins lose their tight association with the Golgi. These defects lead to the incorrect deposition of cell wall components and proteins during pollen tube growth. COG3 and COG8 interact directly with each other, and a structural model of the Arabidopsis COG complex is proposed. We believe that the COG complex helps to modulate Golgi morphology and vesicle trafficking homeostasis during pollen tube tip growth.

Maintaining order: COG complex controls Golgi trafficking, processing, and sorting

“…Conserved oligomeric Golgi deficient plants were not specifically characterized for altered glycosylation, but had impaired cell wall function which could be due to COG‐related glycosylation defects affecting cell wall integrity.…”

“…In worms, COG deficiency affects gonadal formation resulting in reduced proliferation . In plants, COG dysfunction causes a number of dysmorphic phenotypes ranging from alterations in the shoot apical meristem and dwarfed cog7 organisms to male sterility and defects in cell wall components in cog3 and cog8 mutants . The Golgi in the pollen of these plants was dilated and/or fragmented into mini stacks.…”

“…A few different models for the COG complex function during vesicle tethering have been proposed . In each of these models, the COG complex has a central role in orchestrating membrane trafficking but the stage at which the COG complex is involved differs.…”

“…Does the COG complex interact with any other CATCHRs or perform other functions secondary to its primary role in Golgi trafficking? There is some evidence that COG subunits could directly interact with GARP and Exocyst components . Additionally, the COG complex shares SNARE partners with the GARP complex .…”

Hypothesis: lobe A (COG1–4)-CDG causes a more severe phenotype than lobe B (COG5–8)-CDG

“…Cog3-deficient and Cog8-deficient plants Arabidopsis thaliana exhibited short cisternae with increased widths as well as less efficient anterograde trafficking, slow growth and male sterility 13. In the Cog5-deficient fly Drosophila melanogaster , it was observed that the COG complex is necessary for changing the cellular and subcellular morphology during spermatogenesis, again resulting in male sterility 14.…”