Ed

Defects in the three nuclear actin-related proteins (ARP4, ARP6, and ARP7) disrupt the multicellular development of nearly all tissues and organs and alter developmental phase transitions like that from vegetataive to reproducive growth and from apical to lateral shoot and root development. We have published a series of papers on the properties of three nuclear ARPs (ARP4, ARP6, ARP7) demonstrating their essential roles in multicellular development. These data are briefly summarized in the figure below. More recently our efforts have turned to determining the mechistism of chromatin remodeling that alter gene expression to control development.
	Figure Legend: Deficiencies in Arabidopsis actin-related proteins ARP4, ARP6, and ARP7 alter cell proliferation and plant development. From Meagher et al, 2005 review in Plant Physiology. A. Wild-type Arabidopsis plant.  ARP4, 6, and 7 are localized to the interphase nucleus. In mitotic cells lacking intact nuclear membrane (*) they are dispersed throughout the cytoplasm. For example, the insert depicts the subcellular distribution of ARP4 in wild-type root apical cells.  B. Knockout arp7-1 mutation causes homozygous embryo lethality.  Mutant embryos (right) are arrested at the heart (top) or torpedo (bottom) stage of development.  A wild-type embryo at the cotyledon stage from the same silique (fruit) is shown at the left. C. Knocking out or knocking down ARP4, 6, and 7 cause poor seed germination or early seedling development depending upon the level of reduction in the expression of these proteins.  Dwarf ARP4RNAi seedlings (10 d old) with stunted cothledons are shown with two wild-type seedlings (arrow heads) in the upper panel.  Two-week-old normal wild-type (WT) and arrested ARP7RNAi seedlings from a strong line showing more than 85% reduction in ARP7 expression are shown in the lower panel. D. Deficiencies in the expression of ARP4, 6, and 7 affect leaf size, number and/or morphology.  The arp6-1 knockout mutants produce narrow and highly serrated leaves under short-day photoperiod (lower panel).  All the leaves from an adult ARP4RNAi plant are compared with those from wild-type (upper panel). E. SEM of the smaller leaves of ARP7RNAi plants reveal similar number, but smaller sized leaf epidermal cells.  For comparison, knocking out ARP6 in the arp6-1 mutant results in dwarfed leaves with a smaller number of normally sized cells. See Figure 1 at the beginning of this section on epigenetics. F. A knockdown of ARP7 in RNAi plants severely affects root growth.  The retarded roots of RNAi plants have highly reduced cell elongation zone compared to wild-type (WT).	G. Deficiencies in ARP4 and ARP6 expression affect flowering time. ARP4RNAi plants flower early only under long-day conditions (lower panel), whereas, the arp6-1 mutants flower early both under long- and short-day conditions (upper panel).  Thus, ARP4 and ARP6 are involved in photoperiod-dependent and photoperiod-independent flowering pathways, respectively.  H. A knockdown in ARP4 and ARP7 in the RNAi plants causes delayed senescence and abscission of floral organs. Wild-type inflorescences each contain 5 or 6 flowers with intact sepals and petals, whereas the RNAi plants have 15 to 20 flowers in each inflorescence with intact sepals and petals. See Figure 2 at the beginning of this section on epigenetics. I. A strong reduction in ARP4 and ARP7 expression affects stamen development and male fertility.  The aberrant heart-shaped anthers in the arp4-1 mutant contain less pollen than wild-type. J. Deficiencies in ARP4 and ARP6 expression affect female fertility.  Defects in pistil development and pollination results in stunted fruits with reduced seed set compared to wild-type. K. Knocking out or knocking down ARP4, 6, and 7 expression affect flower morphology and/or organ number.

 

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