Figure S1.
Synteny, expression analysis and CSLD alignment. (A) Synteny analysis of CSLD diversification based on the chromosome-scale assembly of the P. patens genome (Lang et al., 2018) shows that CSLD2 and CSLD6 are close paralogs. The eight P. patens CSLDs reside on chromosomes descended from two of the seven chromosomes proposed to have existed before the first of two whole genome duplications (WGD). CSLD2 and 6 diverged from a common ancestor in WGD1. Following WGD2 paralogs of CSLD6 and CSLD2 were lost from chromosomes 5 and 16, respectively. Duplication of the chromosome carrying the common ancestor of CSD1, 3, 4, 5, 7 and 8 in WGD1 was followed by a fusion affecting the common ancestor of chromosomes 1 and 2, which both carry two CSLDs as tandem repeats. The tandem duplication may have occurred after WDG2 on the common ancestor of chromosomes 1 and 2 or before WGD1 followed by loss of one duplicate from the common ancestor of chromosomes 14 and 10/17. There is no evidence of loss following WGD2. Intron structure is most parsimoniously explained by intron loss. CSLD2 and 6 have three introns, the second of which is shared with P. patens CESAs (Roberts and Bushoven, 2007). This intron two is present in CSLD3 and 7, but not CSLD1, 4, 5, and 8 (indicated in red). Gain of intron two in CSLD2, 3, 6, and 7 is unlikely given that it is homologous with an intron in P. patens CESAs. It is possible that intron 2 was lost before WGD2 in the common ancestor of CSLD5 and 8 and lost independently in the common ancestor of CSLD1 and 4 before WGD2, but after tandem duplication of the common ancestor of CSLD1, 3, 4, and 7. Alternatively, tandem duplication and loss of intron two in the common ancestor of CSLD1, 4, 5, and 8 may have occurred before WGD1 with loss of the paralog of the CSLD3 and 7 common ancestor occurring before WGD2. (B) Transcriptional profile of P. patens CSLDs at different developmental stages using a NimbleGene custom microarray (Ortiz-Ramírez et al., 2016) accessed from PEATmoss (Fernandez-Pozo et al., 2020). CSLD2 and CSLD6 had higher expression in gametophores and sporophytes compared to protonemal tissues (chloronema and caulonema). In contrast, the other six P. patens CSLDs were more highly expressed in protonemal tissues and had low expression in gametophores. Results from transcriptional profiling of P. patens developmental stages using a CombiMatrix array (Hiss et al., 2014; Wolf et al., 2010) or RNA-seq (Perroud et al., 2018) were generally consistent, although CSLD2 transcripts were not detected in the RNA-seq analysis. (C) Sequence alignment of PpCESA10 and PpCSLD with Zn-binding domain (blue), transmembrane helices (gray), plant conserved region (aqua), class-specific region (pink), interfacial helix (orange), and conserved D, D, D, QxxRW motifs (red) highlighted based on homology with PttCESA8 (Purushotham et al., 2020). The red circle indicates the location of the TEN mutation. Black circles indicate the locations of point mutations that confer isoxaben resistance in Arabidopsis CESAs. No DCB resistance mutation have been characterized (Larson and McFarlane, 2021).

Synteny, expression analysis and CSLD alignment. (A) Synteny analysis of CSLD diversification based on the chromosome-scale assembly of the P. patens genome (Lang et al., 2018) shows that CSLD2 and CSLD6 are close paralogs. The eight P. patens CSLDs reside on chromosomes descended from two of the seven chromosomes proposed to have existed before the first of two whole genome duplications (WGD). CSLD2 and 6 diverged from a common ancestor in WGD1. Following WGD2 paralogs of CSLD6 and CSLD2 were lost from chromosomes 5 and 16, respectively. Duplication of the chromosome carrying the common ancestor of CSD1, 3, 4, 5, 7 and 8 in WGD1 was followed by a fusion affecting the common ancestor of chromosomes 1 and 2, which both carry two CSLDs as tandem repeats. The tandem duplication may have occurred after WDG2 on the common ancestor of chromosomes 1 and 2 or before WGD1 followed by loss of one duplicate from the common ancestor of chromosomes 14 and 10/17. There is no evidence of loss following WGD2. Intron structure is most parsimoniously explained by intron loss. CSLD2 and 6 have three introns, the second of which is shared with P. patens CESAs (Roberts and Bushoven, 2007). This intron two is present in CSLD3 and 7, but not CSLD1, 4, 5, and 8 (indicated in red). Gain of intron two in CSLD2, 3, 6, and 7 is unlikely given that it is homologous with an intron in P. patens CESAs. It is possible that intron 2 was lost before WGD2 in the common ancestor of CSLD5 and 8 and lost independently in the common ancestor of CSLD1 and 4 before WGD2, but after tandem duplication of the common ancestor of CSLD1, 3, 4, and 7. Alternatively, tandem duplication and loss of intron two in the common ancestor of CSLD1, 4, 5, and 8 may have occurred before WGD1 with loss of the paralog of the CSLD3 and 7 common ancestor occurring before WGD2. (B) Transcriptional profile of P. patens CSLDs at different developmental stages using a NimbleGene custom microarray (Ortiz-Ramírez et al., 2016) accessed from PEATmoss (Fernandez-Pozo et al., 2020). CSLD2 and CSLD6 had higher expression in gametophores and sporophytes compared to protonemal tissues (chloronema and caulonema). In contrast, the other six P. patens CSLDs were more highly expressed in protonemal tissues and had low expression in gametophores. Results from transcriptional profiling of P. patens developmental stages using a CombiMatrix array (Hiss et al., 2014; Wolf et al., 2010) or RNA-seq (Perroud et al., 2018) were generally consistent, although CSLD2 transcripts were not detected in the RNA-seq analysis. (C) Sequence alignment of PpCESA10 and PpCSLD with Zn-binding domain (blue), transmembrane helices (gray), plant conserved region (aqua), class-specific region (pink), interfacial helix (orange), and conserved D, D, D, QxxRW motifs (red) highlighted based on homology with PttCESA8 (Purushotham et al., 2020). The red circle indicates the location of the TEN mutation. Black circles indicate the locations of point mutations that confer isoxaben resistance in Arabidopsis CESAs. No DCB resistance mutation have been characterized (Larson and McFarlane, 2021).

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