Regulation of lipid droplets by metabolically controlled Ldo isoforms

Abstract

Lipid droplets (LDs) are essential organelles for cellular energy homeostasis, but how metabolic cues are integrated in their life cycle is unclear. Teixeira et al. find that two protein isoforms, Ldo16 and Ldo45, differentially regulate LD dynamics under nutrient-rich and -deprived conditions, linking energy metabolism and storage.

The assembly of lipid droplets and their roles in challenged cells

“…Similarly, loss of Ldo16p reduces the number of droplets clustered at the NVJ in stationary phase. Consistent with this, both Ldo45p and Ldo16p are highly expressed in yeast undergoing exponential growth, but only Ldo16p expression is maintained in stationary phase, implying a role for the latter in stationary‐phase droplet dynamics and vacuolar turnover (Teixeira et al , ). Collectively, these studies suggest the spatial distribution of droplets is highly dependent on the metabolic status of the cell, as yeast entering stationary phase exhibit a significant accumulation of NVJ‐associated droplets that associate with the NVJ tether Mdm1p (Hariri et al , ).…”

Lipid droplet–membrane contact sites – from protein binding to function

“…In addition, members of the vacuolar protein sortingassociated protein 13 (Vps13) family have been shown to be involved in ER-LD contacts, possibly to mediate lipid transfer (Kumar et al, 2018); however, whether Vps13 has a partner on LDs has not yet been resolved. Seipin protein partners have been proposed to participate in the interactions of LDs; these include promethin in mammals (Castro et al, 2019), Ldo proteins in yeast (Teixeira et al, 2018;Eisenberg-Bord et al, 2018) and the LDAP proteins in Arabidopsis. Importantly, all these proteins have key roles in LDs biogenesis.…”

Yeast FIT2 homologs mediate the crosstalk between stress response pathways and cellular proteostasis

“…Similar findings were reported in a separate study wherein changes in the acyl chain composition of phospholipids in fld1Δ were hypothesised to drive the formation of large LDs from the fusion of preexisting ones [82]. It was also reported more recently that the expression of the Ldo45 subunit of the Fld1/Ldb16 complex greatly affected the levels of cellular TG, which may yield more direct effects on LD formation [64].…”

“…compartments such as the mitochondria [59][60][61], the vacuole [62][63][64], the proteasome and the autophagic machinery [65,66]. The understanding of this intimate association in turn not only provides support for the involvement of LDs in a wide array of non-metabolic cellular processes such as organellar regulation, autophagy and protein quality control [67][68][69][70] but also alludes to the potential cascade of cellular damage should LD homeostasis be dysregulated.…”