Frameshift mutations generally result in loss-of-function changes since they drastically alter the protein sequence downstream of the frameshift site, besides creating premature stop codons. Here we present data suggesting that frameshift mutations in the C-terminal domain of specific ancestral MADS-box genes may have contributed to the structural and functional divergence of the MADS-box gene family. We have identified putative frameshift mutations in the conserved C-terminal motifs of the B-function DEF/AP3 subfamily, the A-function SQUA/AP1 subfamily and the E-function AGL2 subfamily, which are all involved in the specification of organ identity during flower development. The newly evolved C-terminal motifs are highly conserved, suggesting a de novo generation of functionality. Interestingly, since the new C-terminal motifs in the A- and B-function subfamilies are only found in higher eudicotyledonous flowering plants, the emergence of these two C-terminal changes coincides with the origin of a highly standardized floral structure. We speculate that the frameshift mutations described here are examples of co-evolution of the different components of a single transcription factor complex. 3' terminal frameshift mutations might provide an important but so far unrecognized mechanism to generate novel functional C-terminal motifs instrumental to the functional diversification of transcription factor families.

The floral quartet model of floral organ specification poses that different tetramers of MIKC-type MADS-domain transcription factors control gene expression and hence the identity of floral organs during development. Here, we provide a brief history of the floral quartet model and review several lines of recent evidence that support the model. We also describe how the model has been used in contemporary developmental and evolutionary biology to shed light on enigmatic topics such as the origin of land and flowering plants. Finally, we suggest a novel hypothesis describing how floral quartet-like complexes may interact with chromatin during target gene activation and repression.© 2016. Published by The Company of Biologists Ltd.

以切花月季常见的生理性病害为主线，综述了导致生理性病害产生的温度、水分等环境诱因，相应的赤霉素、细胞分裂素、生长素等内源激素的生理性变化，花器官模型中相关功能基因的异常表达。分析了不适宜的温度环境与内源激素变化之间的关系，并结合月季花器官发育的研究现状，探析花器官特性基因在生理性病害形成中的作用机制，为减少切花月季生理性病害及提高其生产和观赏品质提供理论依据。

重瓣花表现为花瓣数目增加、花瓣褶皱或面积增大, 具有较高的观赏价值和经济价值。该文针对重瓣性状中花瓣或花瓣类似器官数目增多的特点, 综述了模式植物和观赏植物中重瓣花形成的分子机理, 包括参与花瓣数量调控的重要转录因子, 以及miRNAs、DNA甲基化、组蛋白修饰和染色质重塑等表观遗传调控方式, 并在此基础上展望未来的研究方向。

植物花器官的生长发育与温度密切相关,高温会导致花器官畸形及体内激素含量的变化。为探究不同生境配合外施生长素（IAA）对花花柴（Karelinia caspia）花器官发育的影响,测定沙漠和人工绿地2种环境下及外施不同浓度生长素（IAA）的花花柴花器官大小（雌花花柱、雄花花丝）及花器官内激素含量的变化。结果表明,在花苞期合适的温度（27-30℃）能够促进花花柴花器官的生长,而在开花过程中,高温（38-40℃）可促进花花柴柱头伸长进而影响花器官生长,直至发育成熟。外施一定浓度的IAA对花花柴花器官的生长具有促进作用,沙漠环境中,外施0.3 μmol/L的IAA促进作用最明显而人工绿地则为0.1 μmol/L。