## 1 Introduction  
Lodging is one of the major problems preventing the increase of rice yield [1]. In severe cases, yield could be reduced by more than 50% or even fail completely. Moreover, lodging can increase humidity in the canopy and within the population [2], and cause fungal diseases [3] and pre-harvest sprouting, all of which would affect the quality and appearance of rice [1, 4]. It mostly happens in the middle and end rice filling stages [4]. Because the dry organic matter in the stem sheath is continuously transferred to the spikelet, the mechanical strength of the stem sheath weakens with the increase of grain, causing lodging [5]. Rice lodging is classified into three types: bending lodging, frustrated lodging, and torsional lodging [4]. The widespread use of the Green Revolution gene \"_sd1_\" effectively reduced the occurrence of lodging and significantly improved fertility resistance and the harvest index of rice. However, due to the low biomass accumulation of dwarf plants, the utilization rate of population light energy was reduced, which reduced the biological yield and limited the yield improvement [6; 7]. As a result, in the 1990s, the use of strain improvement for ultra-high yield rice breeding and selection of super rice began to achieve yield improvement by increasing the yield of varieties [8; 9; 10]. However, increasing plant height inevitably led to an increase in biological yield, and the problem of lodging resurfaced. The plant height, pushing resistance of the lower part, internode number, internode length, stem diameter, stem wall thickness, vascular bundles and other morphological characteristics all bear relation to rice lodging [11; 12; 13; 14; 15]. Researchers mined and cloned QTLs for a number of lodging-resistant features and conducted biological function investigations. The dwarf genes _sd1_, _d11_, _d14_, _d61_, and _SBI_ played a role in controlling the synthesis and metabolism of hormones such as gibberell (GA) and rapeseed lactone (BR), which primarily altered internode length and stem wall thickness and, consequently, the plant's resistance to lodging [16; 17; 14; 18]. The mutations in the cellulose synthases, which were encoded by _OsCESA4(Bc7)_, _OsCESA7_, and _OsCESA9(Bc6)_, led to the production of defective secondary wall cellulose and decreased stem strength [19; 20; 21; 22]. The mutants of _OsBC17_, which were a novel allele of _TAC4_, have lower lignin content and weak lodging resistance [23]. Reduced cellulose content, thinner secondary cell walls, and decreased mechanical strength of culm were the results of mutations in the kinesin genes _OsDRP2B(Bc3)_, _BC15(OsCTL1)_, and _BC10_[24; 25; 26; 27]. The _OsEXTL_ gene transgenic plants showed remarkably thickened secondary cell walls with higher cellulose levels, resulting in a significant increase in detectable mechanical strength [28]. By boosting cellulose content, the bending-resistant lodging gene _BSUC11_ prevented the physical strength of the upper culm from declining [29]. Furthermore, varieties carrying the ideal plant type gene _IPA1_ frequently exhibited thick culm and a high resistance for lodging [30]. The _OsCAD2_ gene for thick and stiff culm could improve the lodging resistance of lignin-deficient rice varieties [31]. Several known genes for strong culm resistance were involved in culm morphology regulation. _SCMI(Gn1a)_, _SCM2(APOI)_ and _SCM3(OSTBI)_ improved culm structure and increased the plant lodging resistance by increasing stem diameter, stem wall thickness, and the number of mechanical tissue cells [32; 33; 34; 35]. _SBI_ increased the lodging resistance of rice by shortening the length of the basal internodes [17]. _Smos1_ improved resistance to lodging of rice by increasing the number of cells in the stem and stem wall [36].