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. 2009 Jun 15;20(12):2885–2899. doi: 10.1091/mbc.E08-12-1160

Table 1.

Summary of findings

GalT localization phenotype (ER-to-Golgi transport) Golgi scattering phenotype (GM130, GRASP65 labelling) ERGIC structure phenotype (ERGIC-53 labeling) Transferrin-labeled endosome phenotype (peripheral distribution) Abscission phenotype (anaphase bridges) Phospho-histone H3 labeling phenotype (mitotic progression)
Dynein-1 heavy chain, DHC1 (DYNC1H1) NO YES YES YES NO YES
IC2 (DYNC1LI2) NO YES YES YES NO YES
LIC1 (DYNC1LI1) YES YES YES NO NO YES
LIC2 (DYNC1LI2) NO NO NO YES YES YES
Tctex1 (DYNLT1) YES YES NO YES NO YES
rp3 (DYNLT3) NO NO NO NO NO NO
Roadblock 1 (DYNLRB1) NO YES NO YES YES YES
LC8 (DYNLL1) YES NO NO YES YES NO
Dynein-2 heavy chain, DHC2 (DYNC2H1) NO NO NO NO NO NO
D2LIC1, LIC3 (DYNC2LI1) NO NO NO NO NO NO

Defects are summarized here based on visual inspection of images and statistical relevance from automated object quantification. Consequently, as an example, LC8 (DYNLL1) scores negative for Golgi structure because we only see a strong phenotype when using COPI as a marker that also reports ongoing transport between the ER and Golgi. When measured using GM130 or GRASP65-GFP as markers, Golgi structure is not strongly perturbed after LC8 suppression.