QTL mapping identifies novel major loci for kernel row number-associated ear fasciation, ear prolificacy and tillering in maize (Zea mays L.)

Abstract

Maize ear fasciation originates from excessive or abnormal proliferation of the ear meristem and usually manifests as flattened multiple-tipped ear and/or disordered kernel arrangement. Ear prolificacy expresses as multiple ears per plant or per node. Both ear fasciation and prolificacy can affect grain yield. The genetic control of the two traits was studied using two recombinant inbred line populations (B73 × Lo1016 and Lo964 × Lo1016) with Lo1016 and Lo964 as donors of ear fasciation and prolificacy, respectively. Ear fasciation-related traits, number of kernel rows (KRN), ear prolificacy and number of tillers were phenotyped in multi-year field experiments. Ear fasciation traits and KRN showed relatively high heritability (h2 > 0.5) except ratio of ear diameters. For all ear fasciation-related traits, fasciation level positively correlated with KRN (0.30 ≤ r ≤ 0.68). Prolificacy and tillering were not correlated and their h2 ranged from 0.41 to 0.78. QTL mapping identified four QTLs for ear fasciation, on chromosomes 1 (two QTLs), 5 and 7, the latter two overlapping with QTLs for number of kernel rows. Notably, at these QTLs, the Lo1016 alleles increased both ear fasciation and KRN across populations, thus showing potential breeding applicability. Four and five non-overlapping QTLs were mapped for ear prolificacy and tillering, respectively. Two ear fasciation QTLs, qFas1.2 and qFas7, overlapped with fasciation QTLs mapped in other studies and spanned compact plant2 and ramosa1 candidate genes. Our study identified novel ear fasciation loci and alleles positively affecting grain yield components, and ear prolificacy and tillering loci which are unexpectedly still segregating in elite maize materials, contributing useful information for genomics-assisted breeding programs.

Genome-Wide Association Studies on the Kernel Row Number in a Multi-Parent Maize Population

“…The functions of these genes were consistent with those of the GO-and KEGG-enriched pathways. Although previous researchers have identified KRN-associated QTLs on the same chromosomes as in this study [16,85], the physical locations of these KRN-associated QTLs were different. Therefore, we believe that the candidate genes identified in this study are distinct from those reported in previous studies and represent novel candidate genes associated with KRN.…”

Teratogenesis of generative organs of cultivars of Rosa (Rosaceae) in the collection of the M.M. Gryshko National Botanical Garden, National Academy of Sciences of Ukraine

“…Виявлено корелятивні зв'язки між молекулярно-генетичними процесами та морфологічними змінами, які призводять до виникнення фасціацій та інших анoмалій (Meyerowitz et al, 1989;Fletcher, 2002). На думку дослідників, сучасна тератологія як розділ морфології вийшла за межі простого фіксування та опису тератологічних феноменів і перейшла в площину моделювання процесів розвитку та мутаційного аналізу, надаючи корисну інформацію для програм селекції за допомогою геноміки (Li et al, 2023).…”

“…Виявлені тератоморфи підтверджують, що аномалії розвитку та брунькові мутації -це складні фізіологічні процеси, обумовлені порушенням диференціації апікальної меристеми органів рослин, які можуть бути спричинені багатьма факторами: коливанням температури та вологості, дією хімічних і радіоактивних реагентів, патогенними мікроорганізмами (Sim et al, 2004;Yan еt al., 2016;Madhupriya еt al., 2017;Li et al, 2023).…”

Mapping and Functional Analysis of QTL for Kernel Number per Row in Tropical and Temperate–Tropical Introgression Lines of Maize (Zea mays L.)

“…Currently, with the development of molecular marker technologies, genetic localization using GWAS and QTL analysis has been widely used in molecular breeding [10][11][12][13][14]. This has helped reveal the genetic mechanisms of many quantitative traits, such as kernel row number, growth period, KNR, etc., and has facilitated the genetic improvement of these traits [15]. Genes such as inflorescence gene EAD1 [16], Thick tassel dwarf1 (td1) [17], fasciated ear 2 (fea2) and clavate 3/embryo surrounding region-related7 (cle7) [18], compact plant 2 (ct2) [19], fasciated ear3 (fea3) [20], ramose locus2 (rel2) [21], and fon2-like CLE protein 1 (fcp1) [22] can regulate the development of spikelet pair meristems (SPMs) and spike meristems (SMs).…”