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. 2010 Dec;186(4):1497–1502. doi: 10.1534/genetics.110.123661

Figure 1.—

Figure 1.—

lsy-12, a MYST-type histone acetyltransferase, affects ASE laterality. (A) Genes known to be involved in controlling ASEL/R laterality (Hobert 2006; Didiano et al. 2010). (B) Schematic representation of phenotype of representative “2 ASEL” and “2 ASER” mutants. (C) Effects of lsy-12 on ASEL/R laterality markers. A subset of the defects were already reported, upon the initial identification of the lsy-12 locus (Sarin et al. 2007). Numbers below the panels indicate the penetrance of the phenotype, i.e., the fraction of animals that display the phenotype shown in the fluorescent image above. Data on other lsy-12 alleles were reported in Sarin et al. (2007, 2008, 2010). Animals that express the die-1 reporter fosmid also contain a ASEL/R-expressed red fluorescent reporter (che-1∷mCherry) for cell identification. A list of transgenes used in the study is provided in the File S1. Animals were scored as adults. (D) lsy-12 encodes a MYST-type histone acetyltransferase. Analysis of ESTs, expression tiling array clones, PCR specific rescue, and RT–PCR (see File S1 for more details) revealed that R07B5.8 and R07B5.9 are one genetic locus encoding at least two major splice isoforms. The 3′, polyadenylated end of yk82d06 and EX1785569 provide evidence for the existence of the lsy-12b, while other clones provide evidence of the lsy-12a isoform. RT–PCR data suggest that additional splice variants may be produced by the lsy-12 locus (some possibly even including the more upstream predicted gene T11A5.1), but we have not been able to conclusively identify the start and end of such alternative transcripts (data not shown; see also www.wormbase.org). The arrow indicates the predicted translational start site. lsy-12 expression constructs are shown in the lower part of the panel, with the bottom one being a negative control. Staggered red lines indicate that these constructs were generated by in vivo recombineering of co-injected, overlapping PCR fragments (Boulin et al. 2006), some of which were generated by an in vitro PCR fusion approach (Hobert 2002). The generation of constructs is described in File S1. Rescuing data is quantified in Table S1.