Abstract

Cytoplasmic male sterility (CMS) is the failure to produce functional pollen, which is inherited maternally. And it is known that anther development is modulated through complicated interactions between nuclear and mitochondrial genes in sporophytic and gametophytic tissues. However, an unbiased transcriptome sequencing analysis of CMS in cotton is currently lacking in the literature. This study compared differentially expressed (DE) genes of floral buds at the sporogenous cells stage (SS) and microsporocyte stage (MS) (the two most important stages for pollen abortion in JA-CMS) between JA-CMS and its fertile maintainer line JB cotton plants, using the Illumina HiSeq 2000 sequencing platform. A total of 709 (1.8%) DE genes including 293 up-regulated and 416 down-regulated genes were identified in JA-CMS line comparing with its maintainer line at the SS stage, and 644 (1.6%) DE genes with 263 up-regulated and 381 down-regulated genes were detected at the MS stage. By comparing the two stages in the same material, there were 8 up-regulated and 9 down-regulated DE genes in JA-CMS line and 29 up-regulated and 9 down-regulated DE genes in JB maintainer line at the MS stage. Quantitative RT-PCR was used to validate 7 randomly selected DE genes. Bioinformatics analysis revealed that genes involved in reduction-oxidation reactions and alpha-linolenic acid metabolism were down-regulated, while genes pertaining to photosynthesis and flavonoid biosynthesis were up-regulated in JA-CMS floral buds compared with their JB counterparts at the SS and/or MS stages. All these four biological processes play important roles in reactive oxygen species (ROS) homeostasis, which may be an important factor contributing to the sterile trait of JA-CMS. Further experiments are warranted to elucidate molecular mechanisms of these genes that lead to CMS.

Highlights

  • Cytoplasmic male sterility (CMS) is a maternally inherited trait in higher plants incapable of producing functional pollen [1]

  • With 100% sterile plants, JACMS is unique in the following three ways: it has the genetic background of both G. thurberi and G. arboreum; it matures around 20 days earlier than 104-7A [17], another CMS line cultivated by Chinese scientists through backcrossing of G. hirsutum and G. barbadense; it is conditioned by G. hirsutum cytoplasm, which is different from CMS lines of G. harknessii, 104-7A and G. trilobum, CMS-D8, based on origins and phenotypes

  • For JA-CMS and its maintainer line, a floral bud is at the sporogenous cells stage (SS) stage when its diameter is between 1.5–2.2 mm, and at the microsporocyte stage (MS) stage when its diameter reaches 2.2–2.6 mm

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Summary

Introduction

Cytoplasmic male sterility (CMS) is a maternally inherited trait in higher plants incapable of producing functional pollen [1]. CMS plants exhibit normal vegetative growth and female fertility, and this trait can be restored by nuclear genes known as restorer-of-fertility (Rf) genes [2]. It has been widely accepted that CMS is closely related to mitochondrial genome rearrangement, which creates chimeric genes that disturb normal pollen development [3]. More than 50 mitochondrial genes have been identified as CMS-related in various plants [4,5,6,7], which are valuable in producing F1 hybrid cultivars with heterosis. Changes in mitochondrial function trigger altered nuclear gene expression by a mysterious process called mitochondrial retrograde regulation (MRR) [8]. Much is still unknown about signalling pathways involved in this process, MRR targets, and how cells switch to programmed cell death (PCD) mode in the case of CMS

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