Fig. 1

Morphological phenotype of the essp8 mutant. a-c Comparison of seedling phenotypes of WT Col-0 (a) and essp8 mutants (b-c) grown on MS agar for two weeks. The essp8 roots and hypocotyls are shorter and thicker compared to the WT Col-0. d Siliques from a heterozygous parent showing the formation of defective seeds (white arrowheads). e Representative image showing the seedling lethal phenotype in a 3-week-old essp8 mutant. f Image showing the ectopic cell proliferation in a small percentage of mutants (10%). g Ten-day-old WT and essp8 mutant seedlings showing the stunted roots in the mutant. h-i Comparison of the root phenotype between five-day-old WT and essp8 mutant seedlings at the root tip (h) and elongation zone (i) showing abnormally-developed root tips, having bloated cells and formation of short, swollen, and often branched root hairs in the elongation zone. j GSL8 gene structure showing exons (green boxes) and introns (lines). The mutation/insertion sites (red triangles) of alleles used in this work are indicated. The splice site at intron 22 is disrupted in essp8 causing a retention of intron 22 in essp8 which establishes a premature STOP-codon downstream of exon 22. k GSL8 encodes a large transmembrane protein. GSL8 has a large cytoplasmic central loop between the transmembrane domains. The essp8 mutation results in the truncation of the GSL8 protein at the fifth cytoplasmic helix, identified by the red line. Scale bars = 1 mm (a-f), 200 μm (g), 50 μm (h-i)