The shoot apical meristem is a key stem cell niche in plants, and proper stem cell maintenance is partly regulated by CLAVATA3 (CLV3). Without CLV3 meristems overgrow, but the mechanistic basis of this phenotype was unclear. A new paper in Development suggests that CLV3 modulates the physical properties of meristematic stem cells, and that these properties help shape meristem morphology. To learn more about the story behind the paper, we caught up with first author Léa Rambaud-Lavigne and corresponding authors Namrata Gundiah, Arezki Boudaoud and Pradeep Das.

There were errors in Development (2024) 151, dev202216 (doi:10.1242/dev.202216).The incorrect spelling of author name Ritika Ghosal was used. The correct author list appears above.The title and first part of the legend for Fig. 7 were incorrect. The corrected and original titles and legends are shown below:Corrected:Fig. 7. Chemical inhibition of apoptosis partially rescues the Meckel's cartilage defect. (A) Length of Meckel's cartilage in untreated wild type, untreated mutants and 25 µM caspase-treated mutants. Each point represents one side of the lower jaw (Meckel's cartilage). The statistical analyses were conducted using one-way ANOVA followed by Tukey's honest significant difference (HSD) post-hoc test for multiple comparisons, *P<0.05, ****P<0.0001. (B-D) Ventral views of 4 dpf fish, anterior is towards the left. The top and bottom of each box correspond to the third quartile (Q3) and first quartile (Q1), respectively. Each box covers the interquartile range (IQR), where 50% of the data lies. The median is depicted by the horizontal line within each box. The upper whisker extends to the largest value within Q3 + 1.5 * IQR. The lower whisker extends to the smallest value within Q1 - 1.5 * IQR. Any data point outside these whiskers is classified as an outlier. See Mcgill et al. (1978).Original:Fig. 7. Chemical inhibition of autophagy via caspase inhibitor partially rescues the Meckel's cartilage size defect. (A) Graph of linear measurements of Meckel's cartilage length. Each point is one anterior or posterior cartilage, two cartilages per fish. The statistical analyses were conducted using one-way ANOVA followed by Tukey's honest significant difference (HSD) post-hoc test for multiple comparisons, *P<0.05, ****P<0.0001. (B-D) Ventral views of 4 dpf fish, anterior is towards the left. The top and bottom of each box correspond to the third quartile (Q3) and first quartile (Q1), respectively. Each box covers the interquartile range (IQR), where 50% of the data lies. The median is depicted by the horizontal line within each box. The upper whisker extends to the largest value within Q3 + 1.5 * IQR. The lower whisker extends to the smallest value within Q1 - 1.5 * IQR. Any data point outside these whiskers is classified as an outlier. See Mcgill et al. (1978).The legend for Fig. S1 incorrectly stated that z-sections were shown instead of z-projections. The correct legend is shown below:Fig. S1. Fluorescent in-situ hybridization of raptor at 48 hpf. (A-C) Confocal images of double-labeling experiment utilizing wild-type fli1:EGFP fish at 48 hpf, stained with fluorescent in-situ for raptor in red. z-projections are shown, anterior is to the left. Representative images of (A) double-labeled whole body, (B) double-labeled head, and (C) raptor fluorescent in-situ head.The legend for Fig. S4 incorrectly stated that qPCR was shown instead of RT-PCR. The correct legend is shown below:Fig. S4. mTOR pathway genes are maternally provided. RT-PCR of cDNA collected from 2-cell zebrafish embryos.The legend for Fig. S6 was inadvertently repeated for Fig. S7. The correct legend is shown below:Fig. S7. Wild-type and raptor mutants have similar expression patterns of dlx2a, barx1 and nkx3.2. (A-A''') Wild-type and (B-B''') raptor mutant fish at 30 hpf. Fluorescent in-situ hybridization showing (A,B) merged, (A',B')dlx2a(A'',B'')barx1 and (A''',B''')nkx3.2 expression.The authors apologise to the readers for these errors and any inconvenience they may have caused.The online full-text and PDF versions of the paper have been corrected.

The translational stem cell research field has progressed immensely in the past decade. Development and refinement of differentiation protocols now allows the generation of a range of cell types, such as pancreatic β-cells and dopaminergic neurons, from human pluripotent stem cells (hPSCs) in an efficient and good manufacturing practice-compliant fashion. This has led to the initiation of several clinical trials using hPSC-derived cells to replace lost or dysfunctional cells, demonstrating evidence of both safety and efficacy. Here, we highlight successes from some of the hPSC-based trials reporting early signs of efficacy and discuss common challenges in clinical translation of cell therapies.