Replication of newly identified type 2 diabetes susceptible loci in Northwest Indian population

Journal of Cell Biology

Lahr

et al. 2017

Section: Introductionmentioning

confidence: 99%

Cobl-like promotes actin filament formation and dendritic branching using only a single WH2 domain

Journal of Cell Biology

Lahr

et al. 2017

“…Likewise, apart from dendritic branching of neurons studied here, there are no hints on any Cobl roles in functions that the Cobl-like (Cobll-1) gene has been linked to, such as diabetes and obesity ( Mancina et al, 2013 ; Sharma et al, 2017 ). Cobl-like was also suggested as biomarker for different cancer types ( Gordon et al, 2003 ; Gordon et al, 2009 ; Wang et al, 2013 ; Han et al, 2017 ; Plešingerová et al, 2018 ; Takayama et al, 2018 ), to be suppressed by Epstein-Barr virus infection ( Gillman et al, 2018 ) and to be involved in B-cell development ( Plešingerová et al, 2018 ) but there are no hints on Cobl roles in any of these processes.…”

Section: Discussionmentioning

confidence: 79%

Functional interdependence of the actin nucleator Cobl and Cobl-like in dendritic arbor development

Seemann

et al. 2021

eLife

Local actin filament formation is indispensable for development of the dendritic arbor of neurons. We show that, surprisingly, the action of single actin filament-promoting factors was insufficient for powering dendritogenesis. Instead, this required the actin nucleator Cobl and its only evolutionary distant ancestor Cobl-like acting interdependently. This coordination between Cobl-like and Cobl was achieved by physical linkage by syndapins. Syndapin I formed nanodomains at convex plasma membrane areas at the base of protrusive structures and interacted with three motifs in Cobl-like, one of which was Ca2+/calmodulin-regulated. Consistently, syndapin I, Cobl-like’s newly identified N terminal calmodulin-binding site and the single Ca2+/calmodulin-responsive syndapin-binding motif all were critical for Cobl-like’s functions. In dendritic arbor development, local Ca2+/CaM-controlled actin dynamics thus relies on regulated and physically coordinated interactions of different F-actin formation-promoting factors and only together they have the power to bring about the sophisticated neuronal morphologies required for neuronal network formation in mammals.

“…Likewise, apart from dendritic branching of neurons studied here, there are no hints on any Cobl roles in functions that the Cobl-like gene has been linked to, such as diabetes and obesity (Mancina et al, 2013; Sharma et al, 2017). Cobl-like was also suggested as biomarker for different cancer types (Gordon et al, 2003; Gordon et al, 2009; Wang et al, 2013; Han et al, 2017; Plešingerová et al, 2017; Takayama et al, 2018), to be suppressed by Epstein-Barr virus infection (Gillman et al, 2018) and to be involved in B-cell development (Plešingerová et al, 2018) but there are no hints on Cobl roles in any of these processes.…”

Section: Discussionmentioning

confidence: 80%

Functional interdependence of the actin nucleator Cobl and Cobl-like in dendritic arbor development

Seemann

et al. 2021

Preprint

Local actin filament formation is indispensable for development of the dendritic arbor of neurons. We show that, surprisingly, the action of single actin filament-promoting factors was insufficient for powering dendritogenesis. Instead, this process required the actin nucleator Cobl and its only evolutionary distant ancestor Cobl-like acting interdependently. This coordination between Cobl-like and Cobl was achieved by physical linkage by syndapin I. Syndapin I formed nanodomains at convex plasma membrane areas at the base of protrusive structures and interacted with three motifs in Cobl-like, one of which was Ca2+/calmodulin-regulated. Consistently, syndapin I, Cobl-like’s newly identified N terminal calmodulin-binding site and the single Ca2+/calmodulin-responsive syndapin-binding motif all were critical for Cobl-like’s functions. In dendritic arbor development, local Ca2+/CaM-controlled actin dynamics thus relies on regulated and physically coordinated interactions of different F-actin formation-promoting factors and only together they have the power to bring about the sophisticated neuronal morphologies required for neuronal network formation.