Unique Golgi apparatus and vesicle formation in a red alga

Nature ◽  
1976 ◽  
Vol 259 (5544) ◽  
pp. 566-567 ◽  
Author(s):  
RICHARD WETHERBEE ◽  
JOHN A. WEST
1989 ◽  
Vol 141 (4) ◽  
pp. 463-504 ◽  
Author(s):  
George F. Oster ◽  
Louis Y. Cheng ◽  
Hsiao-Ping H. Moore ◽  
Alan S. Perelson

1974 ◽  
Vol 14 (3) ◽  
pp. 633-655
Author(s):  
EVA KONRAD HAWKINS

The fine structure of the Golgi apparatus during development of tetrasporangia of Calli-thamnion roseum is described. Dictyosomes and associated vesicles of 4 developmental stages of sporangia are examined. The wall of sporangia exhibits a heretofore unseen cuticle in red algae. Development of the spore wall and a new plasma membrane around spores occurs through fusion of adjacent Golgi vesicles along the periphery of cells. Observations are discussed in relation to wall formation and expansion of tetrads and in comparison with other work on growth and differentiation of the Golgi apparatus.


2012 ◽  
Vol 86 (18) ◽  
pp. 9675-9682 ◽  
Author(s):  
Meg Trahey ◽  
Hyung Suk Oh ◽  
Craig E. Cameron ◽  
Jesse C. Hay

Poliovirus (PV) requires membranes of the host cell's secretory pathway to generate replication complexes (RCs) for viral RNA synthesis. Recent work identified the intermediate compartment and the Golgi apparatus as the precursors of the replication “organelles” of PV (N. Y. Hsu et al., Cell 141:799–811, 2010). In this study, we examined the effect of PV on COPII vesicles, the secretory cargo carriers that bud from the endoplasmic reticulum and homotypically fuse to form the intermediate compartment that matures into the Golgi apparatus. We found that infection by PV results in a biphasic change in functional COPII vesicle biogenesis in cells, with an early enhancement and subsequent inhibition. Concomitant with the early increase in COPII vesicle formation, we found an increase in the membrane fraction of Sec16A, a key regulator of COPII vesicle formation. We suggest that the early burst in COPII vesicle formation detected benefits PV by increasing the precursor pool required for the formation of its RCs.


1977 ◽  
Vol 58 (2) ◽  
pp. 119-133 ◽  
Author(s):  
Richard Wetherbee ◽  
John A. West
Keyword(s):  

Blood ◽  
2015 ◽  
Vol 125 (22) ◽  
pp. 3509-3516 ◽  
Author(s):  
Marjon J. Mourik ◽  
Frank G. A. Faas ◽  
Hans Zimmermann ◽  
Jan Voorberg ◽  
Abraham J. Koster ◽  
...  

Key Points WPBs stay connected to the Golgi apparatus until vesicle formation is completed. During biogenesis at the Golgi, WPBs increase in size through the addition of nontubular VWF.


2008 ◽  
Vol 180 (4) ◽  
pp. 713-720 ◽  
Author(s):  
Auxiliadora Aguilera-Romero ◽  
Joanna Kaminska ◽  
Anne Spang ◽  
Howard Riezman ◽  
Manuel Muñiz

The p24 family members are transmembrane proteins assembled into heteromeric complexes that continuously cycle between the ER and the Golgi apparatus. These cargo proteins were assumed to play a structural role in COPI budding because of their major presence in mammalian COPI vesicles. However, this putative function has not been proved conclusively so far. Furthermore, deletion of all eight yeast p24 family members does not produce severe transport phenotypes, suggesting that the p24 complex is not essential for COPI function. In this paper we provide direct evidence that the yeast p24 complex plays an active role in retrograde transport from Golgi to ER by facilitating the formation of COPI-coated vesicles. Therefore, our results demonstrate that p24 proteins are important for vesicle formation instead of simply being a passive traveler, supporting the model in which cargo together with a small GTPase of the ARF superfamily and coat subunits act as primer for vesicle formation.


2020 ◽  
Vol 94 (17) ◽  
Author(s):  
J. Fuller ◽  
B. Álvarez-Rodríguez ◽  
E. J. A. A. Todd ◽  
J. Mankouri ◽  
R. Hewson ◽  
...  

ABSTRACT Hazara nairovirus (HAZV) is an enveloped trisegmented negative-strand RNA virus classified within the Nairoviridae family of the Bunyavirales order and a member of the same subtype as Crimean-Congo hemorrhagic fever virus, responsible for fatal human disease. Nairoviral subversion of cellular trafficking pathways to permit viral entry, gene expression, assembly, and egress is poorly understood. Here, we generated a recombinant HAZV expressing enhanced green fluorescent protein and used live-cell fluorescent imaging to screen an siRNA library targeting genes involved in cellular trafficking networks, the first such screen for a nairovirus. The screen revealed prominent roles for subunits of the coat protein 1 (COPI)-vesicle coatomer, which regulates retrograde trafficking of cargo between the Golgi apparatus and the endoplasmic reticulum, as well as intra-Golgi transport. We show the requirement of COPI-coatomer subunits impacted at least two stages of the HAZV replication cycle: an early stage prior to and including gene expression and also a later stage during assembly and egress of infectious virus, with COPI-knockdown reducing titers by approximately 1,000-fold. Treatment of HAZV-infected cells with brefeldin A (BFA), an inhibitor of Arf1 activation required for COPI coatomer formation, revealed that this late COPI-dependent stage was Arf1 dependent, consistent with the established role of Arf1 in COPI vesicle formation. In contrast, the early COPI-dependent stage was Arf1 independent, with neither BFA treatment nor siRNA-mediated ARF1 knockdown affecting HAZV gene expression. HAZV exploitation of COPI components in a noncanonical Arf1-independent process suggests that COPI coatomer components may perform roles unrelated to vesicle formation, adding further complexity to our understanding of cargo-mediated transport. IMPORTANCE Nairoviruses are tick-borne enveloped RNA viruses that include several pathogens responsible for fatal disease in humans and animals. Here, we analyzed host genes involved in trafficking networks to examine their involvement in nairovirus replication. We revealed important roles for genes that express multiple components of the COPI complex, which regulates transport of Golgi apparatus-resident cargos. COPI components influenced at least two stages of the nairovirus replication cycle: an early stage prior to and including gene expression and also a later stage during assembly of infectious virus, with COPI knockdown reducing titers by approximately 1,000-fold. Importantly, while the late stage was Arf1 dependent, as expected for canonical COPI vesicle formation, the early stage was found to be Arf1 independent, suggestive of a previously unreported function of COPI unrelated to vesicle formation. Collectively, these data improve our understanding of nairovirus host-pathogen interactions and suggest a new Arf1-independent role for components of the COPI coatomer complex.


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