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. 2022 Jun 28;13:3701. doi: 10.1038/s41467-022-31282-8

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Scale bar indicates 2 µm. If not stated otherwise, stress was induced by 2 h 2-DG treatment and >200 cells were analyzed for each biologically independent experiment. Values represent percentage of foci formation or co-localization and are shown as mean ± S.D. a Deletion of LSM7 decreases SG formation as compared to the control (his3Δ). Seven biologically independent experiments were examined (unpaired two-tailed t-test). ****p < 0.0001. b Overexpression of LSM7 increases SG formation in the WT (BY4741) strain as compared to empty vector control. No SG induction under unstressed conditions. Six biologically independent experiments were examined (unpaired two-tailed t-test). ****p < 0.0001, ns = 0.3317. c The Pab1 protein expression levels were not changed in the lsm7∆ or the LSM7OE strain. Data are representative of three biologically independent experiments. d Deletion of LSM7 affects SG formation under glucose starvation and stationary phase, as compared to the control (his3∆). Six biologically independent experiments were examined and >300 cells were analyzed for each (unpaired two-tailed t-test). Left to right: ***p = 0.0003, ****p < 0.0001, ns = 0.0519, ns = 0.4126. e Lsm7 foci co-localize with SGs to a greater extent than other Lsm1-7/Pat1 complex components. Three biologically independent experiments were examined (one-way ANOVA followed by Dunnett’s test). Left to right: ****p < 0.0001, ***p = 0.0007, ***p = 0.0003, **p = 0.0018, ***p = 0.001, **p = 0.0036. f Deletion of some Lsm1-7/Pat1 components results in decreased SG formation. Seven (his3Δ, lsm1Δ, pat1Δ), six (lsm6Δ), five (lsm4ΔC), and three (lsm2Δ(TS)) biologically independent experiments were examined (one-way ANOVA followed by Dunnett’s T3 multiple comparisons test, with individual variances computed for each comparison). Left to right: ****p < 0.0001, ns = 0.3105, ns = 0.5875, ns=0.9983, ***p = 0.0006. g Deletion of both LSM7 and LSM1 results in greater loss of SGs than the lsm1Δ single deletion. Seven (lsm1Δ) and three (lsm1Δlsm7Δ) biologically independent experiments were examined (unpaired two-tailed t test with Welch’s correction). **p = 0.003. h Overexpression of LSM8 affects Lsm7 foci and SG formation as compared to empty vector control. Four biologically independent experiments were examined (unpaired two-tailed t test). Left to right: **p = 0.007, ***p = 0.0002, ns = 0.096. Source data are provided as a Source Data file.