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theses

Maize (Zea mays L.) is one of the most important commercial crops in the world as well as an important model organism for basic research in plant biology. The shoot architecture of maize is primarily determined by apical and axillary meristems, specialized groups of stem cells that are responsible for producing branches, lateral organs, and stems. Thus the maintenance and initiation of meristems can directly affect maize reproductive potential and yield. A major goal of my research thesis was to understand the role of different genetic, hormonal and environmental factors in regulating maize shoot growth to shed light on the molecular mechanisms underlying maize architecture.

In the first chapter of my thesis, I contributed to the characterization of the role of auxin signaling in regulating maize architecture by studying two semi-dominant mutants defective in the early stages of reproductive organogenesis, Barren inflorescence1 and Barren inflorescence4 (Bif1 and Bif4). BIF1 and BIF4 encode AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA) proteins, important negative regulators of the auxin signaling pathway. By in situ hybridizations and yeast-2-hybrid screens, I showed that many maize activating AUXIN RESPONSE FACTORs (ARFs) interact with both BIF1 and BIF4 and could potentially play a role in regulating maize inflorescence development. As part of this study, we provided evidence that BARREN STALK1 (BA1), a basic helix-loop-helix (bHLH) transcriptional regulator essential for maize axillary meristem initiation (Gallavotti et al., 2004), is a potential target of auxin signaling. This work has been published in PNAS in 2015 and I was a co-first author (Galli et al., 2015).

In the second chapter of my thesis, we provided new insights into the interplay between inflorescence development and mineral nutrition. Boron is a fundamental micronutrient for plant growth. Previous studies in our lab showed that ROTTEN EAR (RTE), a maize boron efflux transporter, is necessary for maize inflorescence development and fertility (Chatterjee et al., 2014). Here we characterized several RTE-like genes in maize, and showed that the close paralogous gene RTE2, which shares a similar expression pattern with RTE, strongly enhances the rte phenotype in boron deficient conditions, resulting in stunted plants with strong vegetative and reproductive defects. This work showed that in soils with poor boron content both transporter proteins, RTE and RTE2, are necessary to support growth and fertility of maize plants. My main contribution to this study, published in Genetics (Chatterjee et al., 2017), was to characterize the expression of different gene family members.

In the last chapter of my thesis, my research focused on a novel recessive mutant called needle1 (ndl1). ndl1 is a temperature sensitive mutant with variable phenotypic expressivity, showing several defects in development, the most notable of which is the formation of tassels with reduced number of branches and spikelets. Interestingly, ndl1 mutants showed strong genetic interactions with several auxin-related mutants, as well as a lower concentration of auxin in inflorescence meristems. By positional cloning and transgenic complementation, I demonstrated that NDL1 encodes a mitochondrial metalloprotease belonging to the FTSH (FILAMENTOUS TEMPERATURE-SENSITIVE) protease family. In addition, ndl1 mutants showed ROS (reactive oxygen species) hyperaccumulation and strong upregulation of many genes involved in stress responses and mitochondrial retrograde regulation (MRR). Thus the characterization and identification of NDL1 provides new insights into the interaction between redox status and auxin function in meristems, and reveals how genetic and environmental factors contribute to the establishment of maize architecture. With the ongoing warming of our planet, it is more and more important to better understand how crop plants can cope with extreme environments.

ETD_9514

Ph.D.

Includes bibliographical references

by Qiujie Liu

doi:10.7282/t3-2smd-qq43

ETD doctoral

The author owns the copyright to this work.