Ear height is an important maize morphological trait that influences plant lodging resistance in the field, and is based on the number and length of internodes under the ear. To explore the effect of internodes on ear height, the internodes under the ear were analysed in four commercial hybrids (Jinsai6850, Zhengdan958, Xundan20, and Yuyu22) from different heterotic groups in China. The eighth internode, which is the third aboveground extended internode, exhibited high-parent or over high-parent heterosis and contributed considerably to ear height. Thus, the proteome of the eighth internode was examined. Sixty-six protein spots with >1.5-fold differences in accumulation (P < 0.05) among the four hybrids were identified by mass spectrometry and data analyses. Most of the differentially accumulated proteins exhibited additive accumulation patterns, but with epistatic effects on heterosis performance. Proteins involved in phenylpropanoid and benzoxazinoid metabolic pathways were observed to influence indole-3-acetic acid biosynthesis and polar auxin transport during internode development. Moreover, indole-3-acetic acid content was positively correlated with the eighth internode length, but negatively correlated with the extent of the heterosis of the eighth internode length.
Summary
Tubulin folding cofactors (TFCs) are required for tubulin folding, α/β tubulin heterodimer formation, and microtubule (MT) dynamics in yeast and mammals. However, the functions of their plant counterparts remain to be characterized.
We identified a natural maize crumpled kernel mutant, crk2, which exhibits reductions in endosperm cell number and size, as well as embryo/seedling lethality. Map‐based cloning and functional complementation confirmed that ZmTFCB is causal for the mutation.
ZmTFCB is targeted mainly to the cytosol. It facilitates α‐tubulin folding and heterodimer formation through sequential interactions with the cytosolic chaperonin‐containing TCP‐1 ε subunit ZmCCT5 and ZmTFCE, thus affecting the organization of both the spindle and phragmoplast MT array and the cortical MT polymerization and array formation, which consequently mediated cell division and cell growth. We detected a physical association between ZmTFCB and the maize MT plus‐end binding protein END‐BINDING1 (ZmEB1), indicating that ZmTFCB1 may modulate MT dynamics by sequestering ZmEB1.
Our data demonstrate that ZmTFCB is required for cell division and cell growth through modulating MT homeostasis, an evolutionarily conserved machinery with some species‐specific divergence.
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