ratiometric-biosensors-that-measure-mitochondrial-redox-state-atp

Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells

Mitochondria have roles in many cellular processes, from energy metabolism and calcium homeostasis to control of cellular lifespan and programmed cell ...

imaging-mthyper7-ratiometric-biosensor-for-mitochondrial-peroxide

Imaging of mtHyPer7, a Ratiometric Biosensor for Mitochondrial Peroxide, in Living Yeast Cells

Mitochondrial dysfunction, or functional alteration, is found in many diseases and conditions, including neurodegenerative and musculoskeletal disorders, ...

Columbia University

Columbia University Irving Medical Center

Columbia College

Visualization of mitochondria in budding yeast.

Visualisation des mitochondries dans la levure de bi&egrave;re.

Visualizzazione dei mitocondri nel lievito gemmante.

The budding yeast Saccharomyces cerevisiae has many advantages as a model system, but until recently high-resolution microscopy was not often attempted in this organism. Its small size, rounded shape, and rigid cell wall were obstacles to exploring the cell biology of this model eukaryote. However, it is now feasible for laboratories to acquire and analyze high-resolution, multidimensional images of yeast cell biology, including the mitochondria. As a result, imaging of yeast has emerged as an important tool in eukaryotic cell biology. This chapter describes labeling methods and optical approaches for visualizing yeast mitochondria using fluorescence microscopy.

Fluorescence imaging of mitochondria in yeast.

La levure Saccharomyces cerevisiae pr&eacute;sente de nombreux avantages comme un syst&egrave;me mod&egrave;le, mais jusqu&#39;&agrave; ce que la microscopie r&eacute;cemment &agrave; haute r&eacute;solution a &eacute;t&eacute; tent&eacute;e pas souvent chez cet organisme. Sa petite taille, la forme arrondie et la paroi cellulaire rigide &eacute;taient des obstacles &agrave; l&#39;&eacute;tude de la biologie cellulaire de cette eucaryote de mod&egrave;le. Toutefois, il est d&eacute;sormais possible pour les laboratoires d&#39;acqu&eacute;rir et analyser des images &agrave; haute r&eacute;solution, multidimensionnelles de biologie cellulaire et de levure, y compris les mitochondries. Ainsi, l&#39;imagerie de la levure est devenue un outil important dans la biologie de la cellule eucaryote. Ce chapitre d&eacute;crit &eacute;tiquetage des m&eacute;thodes et des approches optiques pour la visualisation des mitochondries de levure &agrave; l&#39;aide de la microscopie de fluorescence.

Imagerie de fluorescence des mitochondries dans la levure.

Il lievito gemmante Saccharomyces cerevisiae ha molti vantaggi come un modello del sistema, ma fino a quando la microscopia ad alta risoluzione recentemente non &egrave; stata tentata spesso in questo organismo. Sue piccole dimensioni, forma arrotondata e rigida parete cellulare sono stati ostacoli per esplorare la biologia cellulare di eucariote questa modello. Tuttavia, ora &egrave; fattibile per i laboratori di acquisire e analizzare le immagini ad alta risoluzione, multidimensionale di biologia delle cellule di lievito, tra cui i mitocondri. Di conseguenza, imaging del lievito &egrave; emerso come uno strumento importante nella biologia delle cellule eucariotiche. Questo capitolo descrive metodi e approcci ottici per visualizzare i mitocondri del lievito utilizzando la microscopia di fluorescenza di etichettatura.

Immagini di fluorescenza di mitocondri in lievito.

This chapter describes labeling methods and optical approaches for live-cell imaging of the cytoskeleton and of a specific organelle-cytoskeleton interaction in budding yeast.

Live-cell imaging of the cytoskeleton and mitochondrial-cytoskeletal interactions in budding yeast.

Ce chapitre d&eacute;crit l&#39;&eacute;tiquetage m&eacute;thodes et approches optiques pour l&#39;imagerie de cellules vivantes du cytosquelette et d&#39;une interaction sp&eacute;cifique organite-cytosquelette dans la levure de bi&egrave;re.

Imagerie de cellules vivantes du cytosquelette et des interactions du cytosquelette-mitochondries dans la levure de bi&egrave;re.

Questo capitolo descrive metodi e approcci ottici per imaging live-cella del citoscheletro e di un&#39;interazione specifico organello-citoscheletro nel lievito gemmante di etichettatura.

Live cell imaging del citoscheletro e interazioni citoscheletriche-mitocondriale nel lievito gemmante.

The budding yeast Saccharomyces cerevisiae has many advantages as a model system, but until recently, high-resolution microscopy was not often attempted in this organism. Its small size, rounded shape, and rigid cell wall were obstacles to exploring the cell biology of this model eukaryote. However, it is now feasible for laboratories to acquire and analyze high-resolution multidimensional images of yeast cell biology. As a result, imaging of yeast has emerged as an important tool in eukaryotic cell biology. This chapter describes labeling methods and optical approaches for visualizing the cytoskeleton and interactions of the actin cytoskeleton with mitochondria in fixed yeast cells using fluorescence microscopy.

Imaging of the cytoskeleton and mitochondria in fixed budding yeast cells.

La levure Saccharomyces cerevisiae pr&eacute;sente de nombreux avantages comme un syst&egrave;me mod&egrave;le, mais jusqu&#39;&agrave; tout r&eacute;cemment, microscopie &agrave; haute r&eacute;solution n&#39;&eacute;tait pas souvent tent&eacute;e dans cet organisme. Sa petite taille, la forme arrondie et la paroi cellulaire rigide &eacute;taient des obstacles &agrave; l&#39;&eacute;tude de la biologie cellulaire de cette eucaryote de mod&egrave;le. Toutefois, il est d&eacute;sormais possible pour les laboratoires acqu&eacute;rir et analyser des images haute r&eacute;solution multidimensionnelles de biologie de cellules de levure. Ainsi, l&#39;imagerie de la levure est devenue un outil important dans la biologie de la cellule eucaryote. Ce chapitre d&eacute;crit &eacute;tiquetage des m&eacute;thodes et des approches optiques pour visualiser le cytosquelette et les interactions entre le cytosquelette d&#39;actine et les mitochondries dans les cellules de levure fixe &agrave; l&#39;aide de la microscopie de fluorescence.

Imagerie du cytosquelette et mitochondries en fixe bourgeonnement des cellules de levure.

Il lievito gemmante Saccharomyces cerevisiae ha molti vantaggi come un modello del sistema, ma fino a poco tempo fa, microscopia ad alta risoluzione non &egrave; stata tentata spesso in questo organismo. Sue piccole dimensioni, forma arrotondata e rigida parete cellulare sono stati ostacoli per esplorare la biologia cellulare di eucariote questa modello. Tuttavia, ora &egrave; fattibile per i laboratori di acquisire e analizzare le immagini ad alta risoluzione multidimensionale di biologia delle cellule di lievito. Di conseguenza, imaging del lievito &egrave; emerso come uno strumento importante nella biologia delle cellule eucariotiche. Questo capitolo descrive metodi e approcci ottici per la visualizzazione del citoscheletro e le interazioni del citoscheletro di actina con i mitocondri nelle cellule di lievito fisso utilizzando la microscopia di fluorescenza di etichettatura.

Imaging del citoscheletro e mitocondri in fissa in erba le cellule di lievito.

Fluorescence loss in photobleaching experiments and analysis of mitochondrial function using superoxide and redox potential biosensors revealed that mitochondria within individual yeast cells are physically and functionally distinct. Mitochondria that are retained in mother cells during yeast cell division have a significantly more oxidizing redox potential and higher superoxide levels compared to mitochondria in buds. Retention of mitochondria with more oxidizing redox potential in mother cells occurs to the same extent in young and older cells and can account for the age-associated decline in total cellular mitochondrial redox potential in yeast as they age from 0 to 5 generations. Deletion of Mmr1p, a member of the DSL1 family of tethering proteins that localizes to mitochondria at the bud tip and is required for normal mitochondrial inheritance, produces defects in mitochondrial quality control and heterogeneity in replicative lifespan (RLS). Long-lived mmr1Î” cells exhibit prolonged RLS, reduced mean generation times, more reducing mitochondrial redox potential and lower mitochondrial superoxide levels compared to wild-type cells. Short-lived mmr1Î” cells exhibit the opposite phenotypes. Moreover, short-lived cells give rise exclusively to short-lived cells, while the majority of daughters of long-lived cells are long lived. These findings support the model that the mitochondrial inheritance machinery promotes retention of lower-functioning mitochondria in mother cells and that this process contributes to both mother-daughter age asymmetry and age-associated declines in cellular fitness.

Mitochondrial quality control during inheritance is associated with lifespan and mother-daughter age asymmetry in budding yeast.

Perte de fluorescence au photoblanchiment exp&eacute;riences et analyse de la fonction mitochondriale &agrave; l&#39;aide de biocapteurs potentiels de superoxyde et d&#39;oxydor&eacute;duction a r&eacute;v&eacute;l&eacute; que les mitochondries dans les cellules de levure individuels sont physiquement et fonctionnellement distinctes. Les mitochondries qui sont conserv&eacute;s dans les cellules de la m&egrave;re pendant la division cellulaire levure ont un potentiel d&#39;oxydor&eacute;duction significativement plus oxydant et des niveaux plus &eacute;lev&eacute;s de superoxyde par rapport aux mitochondries dans les bourgeons. R&eacute;tention des mitochondries avec plus oxydant potentiel r&eacute;dox dans les cellules-m&egrave;res se produit dans la m&ecirc;me mesure dans les cellules jeunes et plus &acirc;g&eacute;s et peut compte du d&eacute;clin &acirc;ge-associ&eacute; total cellulaire mitochondriale potentiel redox chez la levure en vieillissant de 0 &agrave; 5 g&eacute;n&eacute;rations. Suppression de Mmr1p, un membre de la famille DSL1 d&#39;attacher des prot&eacute;ines qui se localise aux mitochondries &agrave; l&#39;extr&eacute;mit&eacute; du bourgeon et est n&eacute;cessaire pour l&#39;h&eacute;ritage mitochondrial normal, produit des d&eacute;fauts de contr&ocirc;le qualit&eacute; mitochondriale et l&#39;h&eacute;t&eacute;rog&eacute;n&eacute;it&eacute; dans la dur&eacute;e de vie r&eacute;plicative (RLS). Mmr1&Delta; longue dur&eacute;e de vie des cellules exposition prolong&eacute;es RLS, r&eacute;duits signifie le temps de g&eacute;n&eacute;ration, plus r&eacute;ductrice de potentiel d&#39;oxydor&eacute;duction mitochondrial et des niveaux inf&eacute;rieurs de superoxyde mitochondriale par rapport aux cellules de type sauvage. Les cellules de mmr1&Delta; courte dur&eacute;e pr&eacute;sentent les ph&eacute;notypes oppos&eacute;s. En outre, cellules &eacute;ph&eacute;m&egrave;res donnent lieu exclusivement aux cellules de courte dur&eacute;es, alors que la majorit&eacute; des filles de cellules longue dur&eacute;e de vie est longtemps v&eacute;cue. Ces r&eacute;sultats confortent le mod&egrave;le que les m&eacute;canismes d&#39;h&eacute;r&eacute;dit&eacute; mitochondriale favorise la r&eacute;tention de bas-fonctionnement des mitochondries dans les cellules de la m&egrave;re et que ce processus contribue &agrave; la fois asym&eacute;trie de l&#39;&acirc;ge de la m&egrave;re-fille et d&eacute;clin &acirc;ge-associ&eacute; de remise en forme cellulaire.

Mitochondrial contr&ocirc;le de la qualit&eacute; au cours de l&#39;h&eacute;ritage est li&eacute; &agrave; l&#39;asym&eacute;trie d&#39;&acirc;ge dur&eacute;e de vie et de la m&egrave;re-fille dans la levure de bi&egrave;re.

Perdita di fluorescenza in photobleaching esperimenti e analisi della funzione mitocondriale usando biosensori potenziali superossido e redox ha rivelato che i mitocondri all&#39;interno delle cellule di lievito individuali sono fisicamente e funzionalmente distinti. I mitocondri che vengono mantenuti in celle della madre durante la divisione delle cellule di lievito hanno un potenziale redox significativamente pi&ugrave; ossidanti e pi&ugrave; elevati livelli di superossido rispetto ai mitocondri nelle gemme. Ritenzione dei mitocondri con pi&ugrave; potenziale redox ossidanti in cellule madre si verifica nella stessa misura in cellule giovani e anziani e pu&ograve; conto per il declino et&agrave;-associate in totale cellulare redox mitocondriali potenziali nel lievito che invecchiano da 0 a 5 generazioni. Eliminazione di Mmr1p, un membro della famiglia DSL1 di legare le proteine che si localizza ai mitocondri presso la punta del germoglio ed &egrave; richiesto per ereditariet&agrave; mitocondriale normale, produce difetti nel controllo qualit&agrave; mitocondriale e l&#39;eterogeneit&agrave; nella durata replicativa (RLS). Mmr1&Delta; lunga vita cellule esposizione prolungata RLS, ridotto significa tempi di generazione, potenziale riduzione redox di mitocondriale pi&ugrave; e pi&ugrave; bassi livelli di superossido mitocondriale rispetto alle cellule wild-type. Breve mmr1&Delta; cellule esibiscono i fenotipi opposti. Inoltre, le cellule di breve durata danno luogo esclusivamente alle cellule di breve durata, mentre la maggior parte delle figlie di cellule longeve &egrave; a lungo vissuta. Questi risultati supportano il modello che il macchinario di eredit&agrave; mitocondriale favorisce la ritenzione di funzionamento inferiore i mitocondri nelle cellule madre e che questo processo contribuisce alla sia asimmetria di et&agrave; della madre-figlia e associate all&#39;et&agrave; declina in fitness cellulare.

Mitocondriale di controllo di qualit&agrave; durante l&#39;ereditariet&agrave; &egrave; associato con durata di vita e madre-figlia asimmetria di et&agrave; nel lievito gemmante.

Mitochondria accumulate at neuronal and immunological synapses and yeast bud tips and associate with the ER during phospholipid biosynthesis, calcium homeostasis, and mitochondrial fission. Here we show that mitochondria are associated with cortical ER (cER) sheets underlying the plasma membrane in the bud tip and confirm that a deletion in YPT11, which inhibits cER accumulation in the bud tip, also inhibits bud tip anchorage of mitochondria. Time-lapse imaging reveals that mitochondria are anchored at specific sites in the bud tip. Mmr1p, a member of the DSL1 family of tethering proteins, localizes to punctate structures on opposing surfaces of mitochondria and cER sheets underlying the bud tip and is recovered with isolated mitochondria and ER. Deletion of MMR1 impairs bud tip anchorage of mitochondria without affecting mitochondrial velocity or cER distribution. Deletion of the phosphatase PTC1 results in increased Mmr1p phosphorylation, mislocalization of Mmr1p, defects in association of Mmr1p with mitochondria and ER, and defects in bud tip anchorage of mitochondria. These findings indicate that Mmr1p contributes to mitochondrial inheritance as a mediator of anchorage of mitochondria to cER sheets in the yeast bud tip and that Ptc1p regulates Mmr1p phosphorylation, localization, and function.

Role for cER and Mmr1p in anchorage of mitochondria at sites of polarized surface growth in budding yeast.

Mitochondries s&#39;accumulent au niveau des synapses neuronales et immunologiques et conseils de bourgeon de levure et associent &agrave; la ER au cours de la biosynth&egrave;se des phospholipides, l&#39;hom&eacute;ostasie du calcium et fission mitochondriale. Ici, nous montrons que les mitochondries sont associ&eacute;s avec des feuilles de ER (cER) corticales sous-jacent de la membrane plasmique dans l&#39;extr&eacute;mit&eacute; du bourgeon et confirment qu&#39;une d&eacute;l&eacute;tion dans YPT11, qui inhibe l&#39;accumulation cER dans l&#39;extr&eacute;mit&eacute; du bourgeon, inhibe &eacute;galement mouillage pointe bourgeon des mitochondries. Time-Lapse imagerie r&eacute;v&egrave;le que les mitochondries sont ancr&eacute;s &agrave; des sites sp&eacute;cifiques &agrave; l&#39;extr&eacute;mit&eacute; du bourgeon. Mmr1p, un membre de la famille DSL1 d&#39;attacher des prot&eacute;ines, localise aux structures ponctu&eacute;es sur surfaces des mitochondries oppos&eacute;es et cER feuilles qui sous-tendent l&#39;extr&eacute;mit&eacute; du bourgeon et est r&eacute;cup&eacute;r&eacute; avec les mitochondries isol&eacute;es et ER. Suppression de MMR1 alt&egrave;re mouillage pointe bourgeon des mitochondries sans affecter la vitesse mitochondriale ou la distribution de cER. Suppression des r&eacute;sultats phosphatase PTC1 dans une augmentation de la phosphorylation Mmr1p, localis&eacute;e des Mmr1p, des d&eacute;fauts dans la liaison de Mmr1p avec les mitochondries et ER et d&eacute;fauts au mouillage de pointe du bourgeon des mitochondries. Ces r&eacute;sultats indiquent que la Mmr1p contribue &agrave; l&#39;h&eacute;r&eacute;dit&eacute; mitochondriale comme m&eacute;diateur d&#39;ancrage des mitochondries &agrave; feuilles cER dans la pointe de bourgeon de levure et que Ptc1p r&eacute;gule la fonction, de localisation et la phosphorylation de Mmr1p.

R&ocirc;le des cER et Mmr1p dans l&#39;ancrage des mitochondries dans les sites de croissance surface polaris&eacute;e dans la levure de bi&egrave;re.

I mitocondri si accumulano a sinapsi neuronali e immunologiche e lievito consigli di bud e associano ER durante la biosintesi di fosfolipidi, omeostasi del calcio e fissione mitocondriale. Qui dimostriamo che i mitocondri sono associati con i fogli di ER (cER) corticale sottostante la membrana plasmatica nella punta del germoglio e confermano che una delezione in YPT11, che inibisce l&#39;accumulo di cER nella punta del germoglio, inibisce anche ancoraggio punta germoglio dei mitocondri. Time-lapse imaging rivela che i mitocondri sono ancorati ai luoghi specifici nella punta del germoglio. Mmr1p, un membro della famiglia DSL1 di legare le proteine, si localizza alle strutture punctate su opposte superfici di mitocondri e cER fogli sottostante la punta del germoglio e viene recuperato con mitocondri isolati ed ER. Eliminazione di MMR1 altera ancoraggio punta germoglio dei mitocondri senza influire sulle velocit&agrave; mitocondriale o distribuzione cER. Eliminazione dei risultati fosfatasi PTC1 aumentata fosforilazione di Mmr1p, mislocalization di Mmr1p, i difetti nell&#39;associazione di Mmr1p con i mitocondri ed ER e difetti di ancoraggio punta germoglio dei mitocondri. Questi risultati indicano che Mmr1p contribuisce all&#39;eredit&agrave; mitocondriale come mediatore di ancoraggio dei mitocondri a fogli cER la punta del germoglio di lievito e che Ptc1p regola la funzione, localizzazione e fosforilazione della Mmr1p.

Ruolo per cER e Mmr1p nell&#39;ancoraggio dei mitocondri in siti di crescita superficiale polarizzata nel lievito gemmante.

Mutations in the lamin A/C gene that cause Hutchinson-Gilford progeria syndrome lead to expression of a truncated, permanently farnesylated prelamin A variant called progerin. Blocking farnesylation leads to an improvement in the abnormal nuclear morphology observed in cells expressing progerin, which is associated with a re-localization of the variant protein from the nuclear envelope to the nuclear interior. We now show that a progerin construct that cannot be farnesylated is localized primarily in intranuclear foci and that its diffusional mobility is significantly greater than that of farnesylated progerin localized predominantly at the nuclear envelope. Expression of non-farnesylated progerin in transfected cells leads to a redistribution of lamin A and lamin C away from the nuclear envelope into intranuclear foci but does not significantly affect the localization of endogenous lamin B1 at nuclear envelope. There is a similar redistribution of lamin A and lamin C into intranuclear foci in transfected cells expressing progerin in which protein farnesylation is blocked by treatment with a protein farnesyltransferase inhibitor. Blocking farnesylation of progerin can lead to a redistribution of normal A-type lamins away from the inner nuclear envelope. This may have implications for using drugs that block protein prenylation to treat children with Hutchinson-Gilford progeria syndrome. These findings also provide additional evidence that A-type and B-type lamins can form separate microdomains within the nucleus.

Blocking farnesylation of the prelamin A variant in Hutchinson-Gilford progeria syndrome alters the distribution of A-type lamins.

Des mutations du g&egrave;ne a/c Lagani&egrave;re qui provoquent le syndrome de Hutchinson-Gilford progeria conduisent &agrave; l&#39;expression d&#39;un tronqu&eacute;, en permanence FARN&Eacute;SYL&Eacute;E prelamin une variante appel&eacute;e progerin. Blocage farnesylation conduit &agrave; une am&eacute;lioration dans la morphologie nucl&eacute;aire anormale observ&eacute;e dans les cellules exprimant progerin, qui est associ&eacute; &agrave; un arrimeur de la variante prot&eacute;ine de l&#39;enveloppe nucl&eacute;aire &agrave; l&#39;int&eacute;rieur du nucl&eacute;aire. Maintenant, nous montrons qu&#39;une construction de progerin qui ne peuvent pas &ecirc;tre FARN&Eacute;SYL&Eacute;E est localis&eacute;e principalement dans les foyers intranucl&eacute;aires et que sa mobilit&eacute; par diffusion est significativement sup&eacute;rieure &agrave; celle de progerin FARN&Eacute;SYL&Eacute;E localis&eacute; surtout &agrave; l&#39;enveloppe nucl&eacute;aire. Expression de progerin non-FARN&Eacute;SYL&Eacute;E dans les cellules transfect&eacute;es conduit &agrave; une redistribution de lamin A et lamine C loin de l&#39;enveloppe nucl&eacute;aire dans des foyers intranucl&eacute;aires mais n&#39;affecte pas significativement la localisation endog&egrave;ne B1 LAGEYRE &agrave; l&#39;enveloppe nucl&eacute;aire. Il y a une redistribution similaire de lamin A et lamin C dans des foyers intranucl&eacute;aires dans des cellules transfect&eacute;es exprimant progerin dans quelle prot&eacute;ine farnesylation est bloqu&eacute; par un traitement avec un inhibiteur de la prot&eacute;ine farnesyltransferase. Blocage farnesylation de progerin peut conduire &agrave; une redistribution des lamines de type normales de l&#39;enveloppe nucl&eacute;aire interne. Cela peut avoir des implications pour l&#39;utilisation de m&eacute;dicaments qui bloquent la pr&eacute;nylation des prot&eacute;ines pour traiter les enfants atteints du syndrome de progeria de Hutchinson-Gilford. Ces r&eacute;sultats fournissent aussi des preuves suppl&eacute;mentaires que lamines de type A et type B peuvent former des microdomaines s&eacute;par&eacute;s dans le noyau.

Blocage farnesylation de l&#39;identification du prelamin une variante dans le syndrome de Hutchinson-Gilford progeria modifie la distribution des lamines de type A.

Mutazioni nel gene della lamina a/c che causano la sindrome di progeria di Hutchinson-Gilford conducono all&#39;espressione di un tronco, permanentemente farnesylated prelamin una variante chiamata progerin. Farnesylation di blocco porta ad un miglioramento nella morfologia nucleare anormale osservato in cellule che esprimono progerin, che &egrave; associato con un re-localization della proteina variante dalla busta nucleare all&#39;interno del nucleare. Mostriamo ora che un costrutto di progerin che non pu&ograve; essere farnesylated &egrave; localizzato principalmente nelle foci intranucleari e che la mobilit&agrave; di diffusione &egrave; significativamente maggiore rispetto a quella di farnesylated progerin localizzata prevalentemente presso la busta nucleare. Espressione di farnesylated non progerin in celle transfected porta ad una ridistribuzione della lamina A e la lamina C dalla busta nucleare in foci intranucleari ma non influisce in modo significativo la localizzazione di endogeno B1 DALI a busta nucleare. C&#39;&egrave; una ridistribuzione simile della lamina A e la lamina C in foci intranucleari nelle celle transfected esprimendo progerin nel quale proteina farnesylation &egrave; bloccato da un trattamento con un inibitore di farnesyltransferase della proteina. Farnesylation di progerin di blocco pu&ograve; portare ad una ridistribuzione del normale tipo lamins lontano dalla busta nucleare interna. Questo pu&ograve; avere implicazioni per l&#39;utilizzo di farmaci che bloccano la prenilazione proteica per trattare i bambini con la sindrome di progeria di Hutchinson-Gilford. Questi risultati forniscono anche ulteriori prove che lamins tipo a e tipo B pu&ograve; formare microdomains separata all&#39;interno del nucleo.

Blocco farnesylation di prelamin una variante nella sindrome di progeria di Hutchinson-Gilford altera la distribuzione di tipo lamins.

Lipid droplets (LDs) have emerged not just as storage sites for lipids but as central regulators of metabolism and organelle quality control. These critical functions are achieved, in part, at membrane contact sites (MCS) between LDs and other organelles. MCS are sites of transfer of cellular constituents to or from LDs for energy mobilization in response to nutrient limitations, as well as LD biogenesis, expansion and autophagy. Here, we describe recent findings on the mechanisms underlying the formation and function of MCS between LDs and mitochondria, ER and lysosomes/vacuoles and the role of the cytoskeleton in promoting LD MCS through its function in LD movement and distribution in response to environmental cues.

ArticleTotal : 2	Year
Publication title Cited by 46	2013
Publication title Cited by 5	2023

Article	Year
Visualization of mitochondria in budding yeast. Methods in cell biology\| PubMed ID: 17445715	2007
Fluorescence imaging of mitochondria in yeast. Methods in molecular biology (Clifton, N.J.)\| PubMed ID: 18314744	2007
Live-cell imaging of the cytoskeleton and mitochondrial-cytoskeletal interactions in budding yeast. Methods in molecular biology (Clifton, N.J.)\| PubMed ID: 19768424	2009
Imaging of the cytoskeleton and mitochondria in fixed budding yeast cells. Methods in molecular biology (Clifton, N.J.)\| PubMed ID: 19768430	2009
Mitochondrial quality control during inheritance is associated with lifespan and mother-daughter age asymmetry in budding yeast. Aging cell\| PubMed ID: 21726403	2011
Role for cER and Mmr1p in anchorage of mitochondria at sites of polarized surface growth in budding yeast. Current biology : CB\| PubMed ID: 22119524	2011
Blocking farnesylation of the prelamin A variant in Hutchinson-Gilford progeria syndrome alters the distribution of A-type lamins. Nucleus (Austin, Tex.)\| PubMed ID: 22895092	2012
Touch and Go: Membrane Contact Sites Between Lipid Droplets and Other Organelles. Frontiers in cell and developmental biology\| PubMed ID: 35281095	2022

Theresa C. Swayne

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