MITD1 is recruited to midbodies by ESCRT-III and participates in cytokinesis

Lee, Seongju; Chang, Jaerak; Renvoisé, Benoît; Tipirneni, Anita; Yang, Shengyuan; Blackstone, Craig

doi:10.1091/mbc.e12-04-0292

Cited by 41 publications

(36 citation statements)

References 33 publications

(54 reference statements)

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“…Generation of stable cell lines. Stable cell lines were generated as described previously (39). For lentiviral experiments, pCMV-dR8.2 dvpr (Addgene) and pCMV-VSV-G (Addgene) were cotransfected into HEK293T cells with the respective pCDH-CMV-MCS-EF1-Puro-based (System Biosciences) constructs.…”

Section: Methodsmentioning

confidence: 99%

Spastic paraplegia proteins spastizin and spatacsin mediate autophagic lysosome reformation

Chang¹,

Lee²,

Blackstone³

2014

J. Clin. Invest.

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187

230

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Autophagy allows cells to adapt to changes in their environment by coordinating the degradation and recycling of cellular components and organelles to maintain homeostasis. Lysosomes are organelles critical for terminating autophagy via their fusion with mature autophagosomes to generate autolysosomes that degrade autophagic materials; therefore, maintenance of the lysosomal population is essential for autophagy-dependent cellular clearance. Here, we have demonstrated that the two most common autosomal recessive hereditary spastic paraplegia gene products, the SPG15 protein spastizin and the SPG11 protein spatacsin, are pivotal for autophagic lysosome reformation (ALR), a pathway that generates new lysosomes. Lysosomal targeting of spastizin required an intact FYVE domain, which binds phosphatidylinositol 3-phosphate. Loss of spastizin or spatacsin resulted in depletion of free lysosomes, which are competent to fuse with autophagosomes, and an accumulation of autolysosomes, reflecting a failure in ALR. Moreover, spastizin and spatacsin were essential components for the initiation of lysosomal tubulation. Together, these results link dysfunction of the autophagy/lysosomal biogenesis machinery to neurodegeneration.

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Section: Methodsmentioning

confidence: 99%

Spastic paraplegia proteins spastizin and spatacsin mediate autophagic lysosome reformation

Chang¹,

Lee²,

Blackstone³

2014

J. Clin. Invest.

Self Cite

187

230

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“…VPS4 is recruited at a late stage during the abscission process through interaction with the ESCRT-III like IST1 protein (Agromayor et al 2009;Bajorek et al 2009), which is negatively regulated by another MIT-domain-containing protein, MITD1 (Hadders et al 2012;Lee et al 2012). It is interesting to note that IST1, while being essential for mammalian cytokinesis, is dispensable for viral budding (Agromayor et al 2009), illustrating a point of divergence between these two ESCRT-III-dependent membrane scission processes.…”

Section: Mechanisms Of Escrt-mediated Membrane Sculptingmentioning

confidence: 99%

Molecular Mechanisms of the Membrane Sculpting ESCRT Pathway

Henne

Stenmark

Emr

2013

Cold Spring Harbor Perspectives in Biology

387

313

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The endosomal sorting complexes required for transport (ESCRT) drive multivesicular body (MVB) biogenesis and cytokinetic abscission. Originally identified through genetics and cell biology, more recent work has begun to elucidate the molecular mechanisms of ESCRTmediated membrane remodeling, with special focus on the ESCRT-III complex. In particular, several light and electron microscopic studies provide high-resolution imaging of ESCRT-III rings and spirals that purportedly drive MVB morphogenesis and abscission. These studies highlight unifying principles to ESCRT-III function, in particular: (1) the ordered assembly of the ESCRT-III monomers into a heteropolymer, (2) ESCRT-III as a dynamic complex, and (3) the role of the AAA ATPase Vps4 as a contributing factor in membrane scission. Mechanistic comparisons of ESCRT-III function in MVB morphogenesis and cytokinesis suggest common mechanisms in membrane remodeling. THE ESCRT PATHWAY IN MVB BIOGENESIS AND CYTOKINESIS

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“…For example, the ESCRT-III protein CHMP1B binds the MIT domains of the AAA ATPase spastin (Figure 4e), which severs microtubules immediately prior to abscission (77). Additional MIT domain-containing proteins recruited by ESCRT-III subunits to function in abscission include the phospholipase D–like protein, MITD1 (CHMP1A, CHMP1B, CHMP2A, and IST1) (177, 178), spartin (SPG20) (IST1) (179), and the protease calpain 7 (IST1:CHMP1B complexes) (180). …”

Section: Biological Functionsmentioning

confidence: 99%

Membrane Fission Reactions of the Mammalian ESCRT Pathway

McCullough

Colf

Sundquist³

2013

Annu. Rev. Biochem.

220

288

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The endosomal sorting complexes required for transport (ESCRT) pathway was initially defined in yeast genetic screens that identified the factors necessary to sort membrane proteins into intraluminal endosomal vesicles. Subsequent studies have revealed that the mammalian ESCRT pathway also functions in a series of other key cellular processes, including formation of extracellular microvesicles, enveloped virus budding, and the abscission stage of cytokinesis. The core ESCRT machinery comprises Bro1 family proteins and ESCRT-I, ESCRT-II, ESCRT-III, and VPS4. Site-specific adaptors recruit these soluble factors to assemble on different cellular membranes, where they carry out membrane fission reactions. ESCRT-III proteins form filaments that draw membranes together from the cytoplasmic face, and mechanistic models have been advanced to explain how ESCRT-III filaments and the VPS4 ATPase can work together to catalyze membrane fission.

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MITD1 is recruited to midbodies by ESCRT-III and participates in cytokinesis

Abstract: The MITD1 is an largely uncharacterized MIT domain–containing protein. This protein localizes to the midbody, with its recruitment dependent on selective interactions with a number of ESCRT-III proteins. These interactions are required for proper abscission.

Cited by 41 publications

References 33 publications

Spastic paraplegia proteins spastizin and spatacsin mediate autophagic lysosome reformation

Spastic paraplegia proteins spastizin and spatacsin mediate autophagic lysosome reformation

Molecular Mechanisms of the Membrane Sculpting ESCRT Pathway

Membrane Fission Reactions of the Mammalian ESCRT Pathway

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