Open Access. Powered by Scholars. Published by Universities.®

Cell Biology Commons

Open Access. Powered by Scholars. Published by Universities.®

Articles 1 - 5 of 5

Full-Text Articles in Cell Biology

A Separable Domain Of The P150 Subunit Of Human Chromatin Assembly Factor-1 Promotes Protein And Chromosome Associations With Nucleoli, Corey L. Smith, Timothy D. Matheson, Daniel J. Trombly, Xiaoming Sun, Eric Campeau, Xuemei Han, John R. Yates Iii, Paul D. Kaufman Sep 2014

A Separable Domain Of The P150 Subunit Of Human Chromatin Assembly Factor-1 Promotes Protein And Chromosome Associations With Nucleoli, Corey L. Smith, Timothy D. Matheson, Daniel J. Trombly, Xiaoming Sun, Eric Campeau, Xuemei Han, John R. Yates Iii, Paul D. Kaufman

Program in Gene Function and Expression Publications and Presentations

Chromatin Assembly Factor-1 (CAF-1) is a three-subunit protein complex conserved throughout eukaryotes that deposits histones during DNA synthesis. Here, we present a novel role for the human p150 subunit in regulating nucleolar macromolecular interactions. Acute depletion of p150 causes redistribution of multiple nucleolar proteins and reduces nucleolar association with several repetitive element-containing loci. Notably, a point mutation in a SUMO-interacting motif (SIM) within p150 abolishes nucleolar associations, whereas PCNA or HP1 interaction sites within p150 are not required for these interactions. Additionally, acute depletion of SUMO-2 or the SUMO E2 ligase Ubc9 reduces alpha-satellite DNA association with nucleoli. The nucleolar ...


Quantitative Proteomic Analysis Reveals Posttranslational Responses To Aneuploidy In Yeast, Noah Dephoure, Sunyoung Hwang, Ciara O'Sullivan, Stacie E. Dodgson, Steven P. Gygi, Angelika Amon, Eduardo M. Torres Jul 2014

Quantitative Proteomic Analysis Reveals Posttranslational Responses To Aneuploidy In Yeast, Noah Dephoure, Sunyoung Hwang, Ciara O'Sullivan, Stacie E. Dodgson, Steven P. Gygi, Angelika Amon, Eduardo M. Torres

Program in Gene Function and Expression Publications and Presentations

Aneuploidy causes severe developmental defects and is a near universal feature of tumor cells. Despite its profound effects, the cellular processes affected by aneuploidy are not well characterized. Here, we examined the consequences of aneuploidy on the proteome of aneuploid budding yeast strains. We show that although protein levels largely scale with gene copy number, subunits of multi-protein complexes are notable exceptions. Posttranslational mechanisms attenuate their expression when their encoding genes are in excess. Our proteomic analyses further revealed a novel aneuploidy-associated protein expression signature characteristic of altered metabolism and redox homeostasis. Indeed aneuploid cells harbor increased levels of reactive ...


Drosophila Sirt2/Mammalian Sirt3 Deacetylates Atp Synthase Beta And Regulates Complex V Activity, Motiur Rahman, Niraj K. Nirala, Alka Singh, Lihua Julie Zhu, Kaori Taguchi, Takeshi Bamba, Eiichiro Fukusaki, Leslie M. Shaw, David G. Lambright, Jairaj K. Acharya, Usha R. Acharya Jul 2014

Drosophila Sirt2/Mammalian Sirt3 Deacetylates Atp Synthase Beta And Regulates Complex V Activity, Motiur Rahman, Niraj K. Nirala, Alka Singh, Lihua Julie Zhu, Kaori Taguchi, Takeshi Bamba, Eiichiro Fukusaki, Leslie M. Shaw, David G. Lambright, Jairaj K. Acharya, Usha R. Acharya

Program in Gene Function and Expression Publications and Presentations

Adenosine triphosphate (ATP) synthase beta, the catalytic subunit of mitochondrial complex V, synthesizes ATP. We show that ATP synthase beta is deacetylated by a human nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, sirtuin 3, and its Drosophila melanogaster homologue, dSirt2. dsirt2 mutant flies displayed increased acetylation of specific Lys residues in ATP synthase beta and decreased complex V activity. Overexpression of dSirt2 increased complex V activity. Substitution of Lys 259 and Lys 480 with Arg in human ATP synthase beta, mimicking deacetylation, increased complex V activity, whereas substitution with Gln, mimicking acetylation, decreased activity. Mass spectrometry and proteomic experiments from ...


Phosphatidic Acid Phospholipase A1 Mediates Er-Golgi Transit Of A Family Of G Protein-Coupled Receptors, Govind Kunduri, Changqing Yuan, Velayoudame Parthibane, Katherine M. Nyswaner, Ritu Kanwar, Kunio Nagashima, Steven G. Britt, Nickita Mehta, Varshika Kotu, Mindy Porterfield, Michael Tiemeyer, Patrick J. Dolph, Usha Acharya, Jairaj K. Acharya Jul 2014

Phosphatidic Acid Phospholipase A1 Mediates Er-Golgi Transit Of A Family Of G Protein-Coupled Receptors, Govind Kunduri, Changqing Yuan, Velayoudame Parthibane, Katherine M. Nyswaner, Ritu Kanwar, Kunio Nagashima, Steven G. Britt, Nickita Mehta, Varshika Kotu, Mindy Porterfield, Michael Tiemeyer, Patrick J. Dolph, Usha Acharya, Jairaj K. Acharya

Program in Gene Function and Expression Publications and Presentations

The coat protein II (COPII)-coated vesicular system transports newly synthesized secretory and membrane proteins from the endoplasmic reticulum (ER) to the Golgi complex. Recruitment of cargo into COPII vesicles requires an interaction of COPII proteins either with the cargo molecules directly or with cargo receptors for anterograde trafficking. We show that cytosolic phosphatidic acid phospholipase A1 (PAPLA1) interacts with COPII protein family members and is required for the transport of Rh1 (rhodopsin 1), an N-glycosylated G protein-coupled receptor (GPCR), from the ER to the Golgi complex. In papla1 mutants, in the absence of transport to the Golgi, Rh1 is ...


Ceramide Transfer Protein Deficiency Compromises Organelle Function And Leads To Senescence In Primary Cells, Raghavendra Pralhada Rao, Luana Scheffer, Sargur M. Srideshikan, Velayoudame Parthibane, Teresa Kosakowska-Cholody, M. Athar Masood, Kunio Nagashima, Prabhakar Gudla, Stephen Lockett, Usha Acharya, Jairaj K. Acharya Mar 2014

Ceramide Transfer Protein Deficiency Compromises Organelle Function And Leads To Senescence In Primary Cells, Raghavendra Pralhada Rao, Luana Scheffer, Sargur M. Srideshikan, Velayoudame Parthibane, Teresa Kosakowska-Cholody, M. Athar Masood, Kunio Nagashima, Prabhakar Gudla, Stephen Lockett, Usha Acharya, Jairaj K. Acharya

Program in Gene Function and Expression Publications and Presentations

Ceramide transfer protein (CERT) transfers ceramide from the endoplasmic reticulum (ER) to the Golgi complex. Its deficiency in mouse leads to embryonic death at E11.5. CERT deficient embryos die from cardiac failure due to defective organogenesis, but not due to ceramide induced apoptotic or necrotic cell death. In the current study we examined the effect of CERT deficiency in a primary cell line, namely, mouse embryonic fibroblasts (MEFs). We show that in MEFs, unlike in mutant embryos, lack of CERT does not lead to increased ceramide but causes an accumulation of hexosylceramides. Nevertheless, the defects due to defective sphingolipid ...