As the first practical cytoplasmic male sterility (cms) system used in hybrid seed production, the first molecularly characterized cms gene and the first cms system for which a restorer was cloned, cms-T and its restorer system have been intensively studied since their identification. The accumulated knowledge on the cms-T system mainly includes: (i) The sterility-causing TURF13 protein is associated with mitochondrial inner membrane. (ii) Both functional alleles of the rf1 and rf2a restorer genes are required to counteract the TURF13's effect and to restore fertility. (iii) rf2a encodes a mitochondrial aldehyde dehydrogenase (ALDH) that is required for fertility restoration. (iv) rf1 interferes with the expression of the T-urf13 gene, and the profile leads to a reduction in the accumulation of TURF13 protein. However, the mechanism that underlines how the mitochondrial TURF13 protein disrupts microspore development and how nuclear restorer genes restore the fertility is not fully understood.;This dissertation is aimed at a better understanding of underlying pathways for fertility restoration and anther development: (i) We used global transcriptome profiling to analyze gene expression in the tapetum, where the action of cms-T and the restoration take place. Prior studies have not been able to focus on this critical single cell layer and all the related data have been based on transcript analysis in either vegetative tissues or mixed reproductive tissues. Our study was able to reveal differentially expressed genes in the tapetal cells of cms plants versus restored plants. (ii) We detected mitochondrial transcripts in our expression profiling analysis and our results suggest that the rf2a nuclear gene affects the stability of T-urf13 transcripts. (iii) We used both forward and reverse genetic approaches to analyze the rso gene, a enhancer of rf2a. Both functional alleles of rf2a and rso are required for normal anther development. Our results establish that rso encodes a maize homologue of mammalian bax inhibitor I that is involved in mitochondrial-mediated programmed cell death (PCD).;In the end, we propose an integrated working hypothesis on the pathways involved in rf2a-mediated fertility restoration in cms-T and in normal anther development.