A developmental delay in the normal expression patterns of multiple genes

Some of the differential Cinoxacin expression may be a temporal shift in developmental appearances of transcripts. Notably, in the case of the TT1 homolog, it appears that the decline in its transcript levels was delayed in the defective seed coats relative to the standard seed coats, thus leading to significant differential expression at the 100�C200 mg seed weight range. This profile is similar to the pattern exhibited by the PRP1 protein in that its decline in expression appears to be slowed. Thus, a developmental delay in the normal expression patterns of multiple genes appeared to be a feature of the effect of this mutation as shown in Figures S6�CS10 and S14�CS15. These shifts may be one of the reasons for significant differential expression at the mid-seed weight range of 100�C200 mg and may indicate that the triggering event occurs at or before the 50 mg seed weight range. We present an overview of genes whose expression was affected by the ����net pattern���� mutation in soybean. Two isolines of different genetic backgrounds were used to understand physiology related to this mutation that causes defective cracks in the seed coats. Twelve samples representing three stages of seed coat development from each of the four lines were subjected to the power of next-generation sequencing to obtain millions of transcript reads that were mapped to all 78,773 high and low confidence gene models of Glycine max. There were approximately 1300 significantly differentially expressed genes affected by this mutation in each isoline pair with 364 in common between the two isolines of different genetic backgrounds. The cell wall structural protein genes including proline-rich proteins and glycine-rich proteins were among the transcripts affected by the mutation as well as a number of transcription factors. Some of the transcript patterns indicate that a developmental shift in timing of gene expression underpins the differential gene expression changes at Benzthiazide mid-maturation as shown by graphical presentation of expression patterns for 82 out of 364 genes that were significantly differentially expressed in both the Clark and Harosoy backgrounds.

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